Evaluation of the in vitro activity of ceragenins against Trichomonas vaginalis
Trichomonosis, caused by the protozoan parasite Trichomonas vaginalis, is a curable sexually transmitted disease that is most commonly encountered worldwide. Increasing importance of trichomoniasis and emerging of resistance against metronidazole lead to search for alternative drugs with different mode of activity. The purpose of this study was to determine in vitro activity of ceragenins (CSA-13, CSA-44, CSA-13, and CSA-138) against the metronidazole-susceptible (ATCC 30001) and metronidazole-resistant (ATCC 50138) strains of T. vaginalis. The effective concentrations were evaluated using two strains of T. vaginalis with different metronidazole susceptibilities (ATCC 30001 and ATCC 50138) in the presence of dilution series of ceragenins in 24-well microtitre assays. Overall, all the ceragenins killed the metronidazole-susceptible (ATCC 30001) and metronidazole-resistant (ATCC 50138) strains of T. vaginalis (p>0.05). With regard to the their effects against the studied strains of T. vaginalis, in order of effectiveness, overall, the ceragenins ordered as CSA-13 (the most effective), CSA-131 and CSA-138 (effective similarly), and CSA-44 (the least effective) (p<0.05). All of the ceragenins reduced the trophozoite numbers of both of studied strains of T. vaginalis with a time- and dose- dependent manner (p<0.05). Although all of the study ceragenins, CSA-13, CSA-44, CSA-13, and CSA-138, killed the studied strains of T. vaginalis. CSA-13 is the leading ceragenin as the most effective anti-trichomonas compound, followed by CSA-131 and CSA-138. They have a potential to have a place in the armemantarium of gynecologic and urologic practice for the management of sexually transmitted diseases.
KeywordsTrichomonas vaginalis ceragenin CSA in vitro
Unable to display preview. Download preview PDF.
- Bozkurt-Guzel C., Savage P.B., Akcali A., Ozbek-Celik B. 2014. Potential synergy activity of the novel ceragenin, CSA-13, against carbapenem-resistant Acinetobacter baumannii strains isolated from bacteremia patients. BioMed Research International DOI: 10.1155/2014/710273Google Scholar
- Fastring D.R., Amedee A., Gatski M., Clark R.A., Mena L.A., Levison J., Schmidt N., Rice J., Gustat J., Kissinger P. 2014. Co-occurrence of Trichomonas vaginalis and bacterial vaginosis and vaginal shedding of HIV-1 RNA. Sexually Transmitted Diseases, 41, 173–179. DOI: 10.1097/OLQ.0000000000000089CrossRefGoogle Scholar
- Figueroa-Angulo E.E., Rendón-Gandarilla F.J., Puente-Rivera J., Calla-Choque J.S., Cárdenas-Guerra R.E., Ortega-López J., Quintas-Granados L.I., Alvarez-Sánchez M.E., Arroyo R. 2012. The effects of environmental factors on the virulence of Trichomonas vaginalis. Microbes and Infection, 14, 1411–1427. DOI: 10.1016/j.micinf.2012.09.004CrossRefGoogle Scholar
- Frasson A.P., Santos O., Duarte M., da Silva Trentin D., Giordani R.B., da Silva A.G., da Silva M.V., Tasca T., Macedo A.J. 2012. First report of anti-Trichomonas vaginalis activity of the medicinal plant Polygala decumbens from the Brazilian semi-arid region, Caatinga. Parasitology Research 110, 2581–2587. DOI: 10.1007/s00436-011-2787-4CrossRefGoogle Scholar
- Hobbs M.M., Lapple D.M., Lawing L.F., Schwebke J.R., Cohen M.S., Swygard H., Atashili J., Leone P.A., Miller W.C., Seña A.C. 2006. Methods for detection of Trichomonas vaginalis in the male partners of infected women: implications for control of trichomoniasis. Journal Clinical Microbiology, 44, 3994–3999. DOI: 10.1128/JCM.00952-06CrossRefGoogle Scholar
- Kirkcaldy R.D., Augostini P., Asbel L.E., Bernstein K.T., Kerani R.P., Mettenbrink C.J., Pathela P., Schwebke J.R., Secor W.E., Workowski K.A., Davis D., Braxton J., Weinstock H.S. 2012. Trichomonas vaginalis antimicrobial drug resistance in 6 US cities, STD Surveillance Network, 2009–2010. Emerging Infectious Diseases 18:939–943. DOI: 10.3201/eid1806.111590CrossRefGoogle Scholar
- Leitsch D., Burgess A.G., Dunn L.A., Krauer K.G., Tan K., Duchêne M., Upcroft P., Eckmann L., Upcroft J.A. 2011. Pyruvate:ferredoxin oxidoreductase and thioredoxin reductase are involved in 5-nitroimidazole activation while flavin metabolism is linked to 5-nitroimidazole resistance in Giardia lamblia. Antimicrobial Agents and Chemotherapy 66, 1756–1765. DOI: 10.1093/jac/dkr192CrossRefGoogle Scholar
- Munson K.L., Napierala M., Munson E., Schell R.F., Kramme T., Miller C., Hryciuk J.E. 2013. Screening of male patients for Trichomonas vaginalis with transcription-mediated amplification in a community with a high prevalence of sexually transmitted infection. Journal Clinical Microbiology, 51, 101–104. DOI: 10.1128/JCM.02526-12CrossRefGoogle Scholar
- Pal D., Banerjee S., Cui J., Schwartz A., Ghosh S.K., Samuelson J. 2009. Giardia, Entamoeba, and Trichomonas enzymes activate metronidazole (nitroreductases) and inactivate metronidazole (nitroimidazole reductases). Antimicrobial Agents and Chemotherapy 53, 458–464. DOI: 10.1128/AAC.00909-08CrossRefGoogle Scholar
- Pollard J.E., Snarr J., Chaudhary V., Jennings J.D., Shaw H., Christiansen B., Wright J., Jia W., Bishop R.E., Savage P.B. 2012. In vitro evaluation of the potential for resistance development to ceragenin CSA-13. Antimicrobial Agents and Chemotherapy 67:2665–2672. DOI: 10.1093/jac/dks276CrossRefGoogle Scholar
- Sobel J.D. 2014. Trichomoniasis. In: UpToDate, Post TW (Ed), Up- ToDate, Waltham, MA. (Accessed on June, 2014)Google Scholar
- WHO 2008. World Health Organization - global prevalence and incidence of selected curable sexually transmitted infections. WHO, Geneva SwitzerlandGoogle Scholar