Peer-reviewed veterinary case report
Vaccine plasmid without antibiotic resistance triggers dog immunity
By Ramos, I et al.·Published in Vaccine·2009·Centro de Investigaciones Bioló, Spain·View original on PubMed →
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Original publication title: Antibiotic resistance free plasmid DNA expressing LACK protein leads towards a protective Th1 response against Leishmania infantum infection.
- Species:
- dog
Plain-English summary
A study tested a new vaccine for dogs against Leishmania infantum, which causes a serious disease called canine visceral leishmaniasis. The vaccine, made from a plasmid without antibiotic resistance genes, was given to dogs and showed promising results. It reduced symptoms and the number of parasites in the liver, while also boosting the immune response. This suggests that the new vaccine could be an effective way to protect dogs from this disease in areas where it is common.
People also search for: dog leishmaniasis vaccine · canine visceral leishmaniasis treatment · how to protect dog from Leishmania infection
Abstract
Canine visceral leishmaniasis is a serious public health concern in the Mediterranean basin since dogs are the main Leishmania infantum reservoir. However, there is not a vaccination method in veterinary use in this area, and therefore the development of a vaccine against this parasite is essential for the possible control of the disease. Previous reports have shown the efficacy of heterologous prime-boost vaccination with the pCIneo plasmid and the poxvirus VV (both Western Reserve and MVA strains) expressing L. infantum LACK antigen against canine leishmaniasis. As pCIneo-LACK plasmid contains antibiotic resistance genes, its use as a profilactic method is not recommended. Hence, the antibiotic resistance gene free pORT-LACK plasmid is a more suitable tool for its use as a vaccine. Here we report the protective and immunostimulatory effect of the prime-boost pORT-LACK/MVA-LACK vaccination tested in a canine experimental model. Vaccination induced a reduction in clinical signs and in parasite burden in the liver, an induction of the Leishmania-specific T cell activation, as well as an increase of the expression of Th1 type cytokines in PBMC and target organs.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/19747996/