The factors driving host–pathogen interactions in Mccp are not well understood. Consequently, an improved model to reproduce CCPP would not only enable vaccine efficacy studies but also foster in vivo studies that provide insights regarding the molecular mechanisms associated with pathogenicity and the virulence traits involved. The latter two infection methods are technically challenging and can result in different pathomorphological outcomes ranging from the absence of any clinical or pathomorphological changes to severe clinical disease and pathology. Although mimicking the natural disease transmission, in-contact experiments are often time-consuming, require a large number of animals and are difficult to standardize. Past infection models for CCPP include in-contact challenge, endobronchial inoculation and intratracheal administration. The development of an efficacious vaccine formula against CCPP requires a robust and reproducible experimental challenge model. Despite inducing immunity for up to 1 year, the use of a bactericidal adjuvant prohibits the inclusion of this vaccine in a combinatorial formula with live attenuated vaccines against additional caprine diseases such as PPR and capripox. capripneumoniae type strain F38 T and saponin was developed for disease control in domestic goats. During the last century, a bacterin-type of vaccine, co-formulating M. This might be due to lack of disease awareness, declining public funds to conduct surveillance and monitoring, suboptimal diagnostics and a possible misperception of CCPP symptoms with other respiratory diseases such as “peste des petits ruminants” (PPR) or Pasteurella spp. Despite the fact that CCPP is on the list of diseases notifiable to the World Organization for Animal Health (OIE), only a few countries reported outbreaks between 20 (Figure 1). capripneumoniae to wild ungulates such as Arabian Oryx and Tibetan antelope has also been reported. The infection is acquired through inhalation of contaminated droplets and can cause morbidities and mortalities up to 100% and 80%, respectively. capripneumoniae ( Mccp) causes pneumonia with respiratory symptoms that may progress into a lethal, generalized acute pleuropneumonia or to a chronic form with milder clinical signs and restricted pathomorphological lesions. Infection of goats with the causative agent Mycoplasma capricolum subsp. These results will pave the way for a better understanding of host–pathogen interactions during CCPP and subsequent vaccine development.Ĭontagious caprine pleuropneumonia (CCPP) is an important livestock disease that is widespread in the Middle East, Asia and Africa. Peroxide production could be inhibited with serum from convalescent animals. In addition, the function of the glycerol metabolism was verified by measurement of production of H 2O 2 in medium containing physiological serum concentrations of glycerol. Furthermore, the expression of L-α-glycerophosphate oxidase (GlpO) in vivo was confirmed. 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 2O 2) production in the phylogenetically related pathogen M. 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. 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. 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. capripneumoniae is a severe disease widespread in Africa and Asia. Contagious caprine pleuropneumonia (CCPP), caused by Mycoplasma capricolum subsp.
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