Characterization of a Trypanosoma rangeli Strain of Colombian Origin

Zúñiga, Claudio Gandarias; Palau, Teresa; Pénin, P.; Gamallo, Carlos; Diego, J. A. de

doi:10.1590/s0074-02761997000400015

Cited by 8 publications

(4 citation statements)

References 21 publications

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“…A total of 5–10 insects were grouped in small jars, which were then placed under a membrane feeder containing defibrinated, de-complemented human blood (heated to 37·5 °C) supplemented with inactivated FBS with an estimated concentration of 3·3–3·5 × 10 6 parasites/mL. This concentration falls within (a) the range of peak parasitaemias observed in mice and guinea pigs experimentally infected with T. cruzi (Bice and Zeledon, 1970; Urdaneta-Morales and Rueda, 1977; Perlowagora-Szumlewicz and Muller, 1982; Schaub and Losch, 1989 a ; Schaub et al 1989; Kollien et al 1998) and T. rangeli (Urdaneta-Morales and Tejero, 1986; Zuñiga et al 1997 a , b ), and oral infectious doses used in prior published studies of T. cruzi and T. rangeli infection in triatomines (Garcia et al 1994, 2004; Mello et al 1996; Ratcliffe et al 1996; Whitten et al 2001; Borges et al 2006; Araújo et al 2007, 2014; Nogueira et al 2007; Mejía-Jaramillo et al 2009; Ferreira et al 2010; Castro et al 2012, 2014; Fellet et al 2014). Trypanosoma cruzi–T.…”

Section: Methodssupporting

confidence: 61%

Trypanosoma cruzi–Trypanosoma rangelico-infection ameliorates negative effects of single trypanosome infections in experimentally infectedRhodnius prolixus

et al. 2016

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Trypanosoma cruzi, causative agent of Chagas disease, co-infects its triatomine vector with its sister species Trypanosoma rangeli, which shares 60% of its antigens with T. cruzi. Additionally, T. rangeli has been observed to be pathogenic in some of its vector species. Although T. cruzi-T. rangeli co-infections are common, their effect on the vector has rarely been investigated. Therefore, we measured the fitness (survival and reproduction) of triatomine species Rhodnius prolixus infected with just T. cruzi, just T. rangeli, or both T. cruzi and T. rangeli. We found that survival (as estimated by survival probability and hazard ratios) was significantly different between treatments, with the T. cruzi treatment group having lower survival than the co-infected treatment. Reproduction and total fitness estimates in the T. cruzi and T. rangeli treatments were significantly lower than in the co-infected and control groups. The T. cruzi and T. rangeli treatment group fitness estimates were not significantly different from each other. Additionally, co-infected insects appeared to tolerate higher doses of parasites than insects with single-species infections. Our results suggest that T. cruzi-T. rangeli co-infection could ameliorate negative effects of single infections of either parasite on R. prolixus and potentially help it to tolerate higher parasite doses.

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Section: Methodssupporting

confidence: 61%

Trypanosoma cruzi–Trypanosoma rangelico-infection ameliorates negative effects of single trypanosome infections in experimentally infectedRhodnius prolixus

et al. 2016

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“…In contrast, the Colombian C23 strain of T. rangeli showed high infection rates in Vero and J774 cells and an increasing number of amastigote forms after the 8th day of infection as a result of intracellular multiplication (ZunÄ iga et al 1997a). High metacyclogenesis rates were observed when T. rangeli was cultivated on a feeder layer of mouse ®broblasts cells at 27°C, but no ®broblast infection was observed (Tanoura et al 1999).…”

Section: Discussionmentioning

confidence: 94%

Interaction of Trypanosoma rangeli Tejera, 1920 with different cell lines in vitro

Eger-Mangrich

Oliveira

Grisard

et al. 2001

Parasitology Research

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Intracellular multiplication of Trypanosoma rangeli was evaluated in vitro using experimental infection of Vero cells, murine macrophages, and promonocytes with T. rangeli Choachi, Macias, and SC-58 clone B1 strains. Our results revealed a low infectivity of all T. rangeli strains to these cell lines. Macrophages showed the highest infection rate; however, intracellular forms were no longer observed 48 h post infection Despite the observation of intracellular parasites up to 144 h post infection, the infection rates of Vero cells and J774G.8 promonocytes with these parasite strains were always below 5%. Pre-incubation of parasites with normal mouse serum increased the initial infectivity but not the time course of the infection. Under our experimental conditions, we did not observe any evidence of intracellular multiplication of T. rangeli within these cell lines.

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“…PCR amplification, cloning and nucleotide sequence -PCR was performed using TrF1 (5' -CGC CCC GTC TTG CCC TGT-3') and TrR2 (5' -CGC AGC AAG GAC AGG AGG GA-3') primers, which, based on the T. rangeli KP1(-) C23 (MAOT/CO/82/C23) (Zuñiga et al 1997) strain, amplify a 620 bp fragment exclusively in T. rangeli. A 25 µL reaction contained 100 ng purified genomic DNA, 1X reaction buffer (10 mM Tris-HCl pH 9.0, 50 mM KCl and 0.1% Triton X-100), 1.25 units of Expand High Fidelity enzyme (Roche, Branford, USA), 1.5 mM MgCl 2 , 0.2 mM of each deoxynucleoside triphosphate and 20 pmol of each primer.…”

Section: Methodsmentioning

confidence: 99%

Cl gene cluster encoding several small nucleolar RNAs: a comparison amongst trypanosomatids

Nocua

Gómez

Cuervo

et al. 2009

Mem. Inst. Oswaldo Cruz

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Characterization of a Trypanosoma rangeli Strain of Colombian Origin

Cited by 8 publications

References 21 publications

Trypanosoma cruzi–Trypanosoma rangelico-infection ameliorates negative effects of single trypanosome infections in experimentally infectedRhodnius prolixus

Trypanosoma cruzi–Trypanosoma rangelico-infection ameliorates negative effects of single trypanosome infections in experimentally infectedRhodnius prolixus

Interaction of Trypanosoma rangeli Tejera, 1920 with different cell lines in vitro

Cl gene cluster encoding several small nucleolar RNAs: a comparison amongst trypanosomatids

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