The impact of asymptomatic carriers on the survival of Mycoplasma bovis in the environment and the role of wildlife in transmitting M. bovis still requires to be extensively studied. In this study, we have extended the arsenal of factors implicated in pathogenicity of M. bovis to shed light on the current knowledge gap. A number of 460 lung samples (pneumonic; n=210 and apparently healthy; n=250) were randomly collected from one hundred humped camels (Camelus domedarius). Biochemically, 13/210 of the recovered isolates (27.3%) from the pneumonic lungs were recorded as putative mycoplasmas and to be confirmed by PCR to be M. bovis. Infection with M. bovis was not detected in the apparently healthy lungs. They were examined for their phenotypic virulence traits and antimicrobial resistance. Haemolysis and hydrogen sulphide (H2S) production was evident in 100% of the isolates. All 13 M. bovis isolates were weak in their ability to form biofilm on polystyrene surfaces and were 100% susceptible to florfenicol, spiromycin and streptomycin while 100% resistant to ciprofloxacin. Five different combinations of antibiotics representing one to three classes with the Macrolide erythromycin being the most represented. Surprisingly, we did not detect the uvrC and gapA virulence genes by PCR, however we did detect the vsp gene in 2 out of 13 isolates. In addition, we detected the parC gene encoding quinolone resistance in 2 out of 13 M. bovis isolates, but did not detect the gyrA gene. Moreover, we have showed H2S, a compound that has previously not been identified as a virulence factor in M. bovis.