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Contagious caprine pleuropneumonia (CCPP), caused by  Mycoplasma capricolum  subsp.  capripneumoniae  is a severe disease widespread in Africa and Asia. Limited knowledge is available on the pathogenesis of this organism, mainly due to the lack of a robust in vivo challenge model and the means to do site-directed mutagenesis. This work describes the establishment of a novel caprine challenge model for CCPP that resulted in 100% morbidity using a combination of repeated intranasal spray infection followed by a single transtracheal infection employing the recent Kenyan outbreak strain ILRI181. Diseased animals displayed CCPP-related pathology and the bacteria could subsequently be isolated from pleural exudates and lung tissues in concentrations of up to 10 9  bacteria per mL as well as in the trachea using immunohistochemistry. Reannotation of the genome sequence of ILRI181 and F38 T  revealed the existence of genes encoding the complete glycerol uptake and metabolic pathways involved in hydrogen peroxide (H 2 O 2 ) production in the phylogenetically related pathogen  M. mycoides  subsp.  mycoides . Furthermore, the expression of L-α-glycerophosphate oxidase (GlpO) in vivo was confirmed. In addition, the function of the glycerol metabolism was verified by measurement of production of H 2 O 2  in medium containing physiological serum concentrations of glycerol. Peroxide production could be inhibited with serum from convalescent animals. These results will pave the way for a better understanding of host–pathogen interactions during CCPP and subsequent vaccine development.   Electronic supplementary material  The online version of this article (10.1186/s13567-019-0628-0) contains supplementary material, which is available to authorized users.

Reproduction of contagious caprine pleuropneumonia reveals the ability of convalescent sera to reduce hydrogen peroxide production in vitro