What exactly is ID?

The problem is you are referring to genes which apply to disease resistance. The diseases in question rely on the target cells to be functioning normally, so by necessity any resistance mechanism is going to affect normal function.However, I read of an example recently posted by PZ myers in his blog on the evolution of alpha-actinin which anchors the actin cytoskeleton of cells. To describe it briefly, invertebrates have one of these genes whereas vertebrates have four. These extra genes resulted from a duplication event 200-300 million years ago. In that time these duplicated genes have undergone mutations, adapting to subtly different roles, in particular alpha-actinin 2 and 3 which are expressed almost exclusively in skeletal muscle tissue. So how does this fit into your hypothetical genetic entropy?

Of course the ribosome binds to something else. It binds to mRNA and the anti-codons of tRNA carrying amino acids, in it's role of protein synthesis. Streptomycin interferes with the normal role of the ribosome by irreversibly binding to it. This is why streptomycin is an antibiotic, since without protein synthesis the bacterial cell dies, and why it is ridiculous to describe the failure to bind streptomycin as a loss of function. The relevant mutation allows the ribosome to continue functioning in protein synthesis even in the presence of streptomycin, which can be described as a gain in function.