Clinical and immunopathological findings during long term follow-up in Leishmania infantum experimentally infected dogs. Issue 1 (December 2017)

• Record Type: Journal Article
• Authors: Abbehusen, Melissa; Almeida, Valter; Solcà, Manuela; Pereira, Laís; Costa, Dirceu; Gil-Santana, Leonardo; Bozza, Patricia; Fraga, Deborah; Veras, Patrícia; dos-Santos, Washington; Andrade, Bruno; Brodskyn, Claudia
• Is Part Of: Scientific reports. Volume 7:Issue 1(2017)
• Page Start: 1
• Page End: 11
• Publication Date: 2017-12
• Subjects: Natural history -- Research -- Periodicals; Biology -- Research -- Periodicals; Physical sciences -- Research -- Periodicals; Earth sciences -- Research -- Periodicals; Environmental sciences -- Research -- Periodicals; 502.85
• DOI: 10.1038/s41598-017-15651-8
• Languages: English
• ISSNs: 2045-2322

Abstract

Abstract Canine Visceral Leishmaniasis (CVL) is caused byLeishmania infantum, which in the New World is transmitted byLutzomyia longipalpis . While prospective clinical and immunological assessments of dogs experimentally challenged withL. infantum have been previously reported over a relatively short follow-up period, the long-term characterization of infected animals has not been performed to date. We evaluated dogs in a subclinical state for six years following experimental infection withL. infantum andLu. longipalpis saliva, via an intradermal route, to characterize clinical, parasitological and immunological parameters arising fromL. infantum experimental infection. We also assess these parameters in a group of naturally infected animals. The immune profiles of the experimentally and naturally infected animals exhibited increases of IFN-γ, IL-6 and IL-18, and decreases in TNF, IL-2, IL-8 and CXCL1, compared to controls. Our results indicate that over a six-year follow-up post-challenge, subclinically infected dogs presented low CVL clinical scores despite the persistence ofLeishmania parasites in the lymph nodes, spleen and skin. Similarities observed among immune profiles in the context of experimental and natural infection seem to suggest that an enduring activation of the host immune response may lead to the control of parasite growth, thereby limiting disease severity.