Many other products have attained only modest success, in part because of relatively low virulence (high inoculum loads have to be applied) and overall poor and unpredictable performance under field conditions (Thomas 1999).
While a clear reason for this phenomenon is not apparent, it can be speculated that low background attack rates may result from either relatively high pre-existing population resistance to the circulating strain(s), or modest intrinsic virulence of the circulating strains, such that only intense exposures lead to disease.
These observations i.e., lack of a role for hlgABC in USA300 survival after phagocytosis and modest contribution to virulence in the mouse may seem at variance, but might be explained by differences in toxin production and accumulation.
These selection criteria, although sufficient to select strains with superior replicative fitness and, therefore, transmissibility, could also tolerate modest levels of virulence.
Gamma-hemolysin subunits are highly upregulated by USA300 in blood, although the toxin may only have a modest contribution to virulence (Malachowa et al. 2011).
Although the reduction in virulence was modest, this can likely be attributed to the multitude of virulence factors involved in the pathogenesis of staphylococcal endocarditis.
Although a swine-origin H1N1 virus has emerged to become pandemic, its virulence for humans remains modest in comparison to that seen in zoonotic H5N1 disease.
However, the high dose of inoculation used may not allow for discerning more modest contributions of the pilus structures to the virulence of this pathogen.
The modest contribution of gamma-hemolysin to S. aureus virulence is consistent with observations made in previous studies of the role of gamma-hemolysin in animal infection models [33], [34].
Although a swine origin influenza H1N1 virus (H1N1pdm) has recently emerged to become pandemic, its virulence for humans so far remains modest in comparison with that seen in zoonotic H5N1 disease [2].
