If we assume all of these things could be practically done at least at some point in the future, here are the problems I see with the suggestions, and why they might not work (others may spot additional ones).
1 Translocation of a sabotaging 'agent' via the conjugation apparatus.
This basically already exists, look up the various secretion systems of bacteria. In particular, the Type 6 Secretion System does exactly this (though with a somewhat limited target range).
The first paragraph on wiki summarises:
The type VI secretion system (T6SS) is molecular machine used by a wide range of Gram-negative bacterial species to transport proteins from the interior (cytoplasm or cytosol) of a bacterial cell across the cellular envelope into an adjacent target cell.
The reason this wouldn't work is that bacteria have already evolved to deal with such mechanisms, and one we engineer is unlikely to fare much differently.
You can take it from me (as my PhD concerns exactly this!) that changing what the secretion systems translocate, while possible, is very difficult.
2 Phony conjugation
Antibiotics tend to be small molecules. They bind and dock with enzymes or substrates in order to inhibit some kind of activity typically, e.g. cell wall synthesis in the case of Beta-lactam antibiotics such as penicillin. I'm not sure how you imagine it would "tear a hole in the bacterium" really?
Related to the T6SS, are R-type Pyocins, which are co-opted bacteriophages that sort of do this. It requires no conjugation, and the currently proposed mechanism is that they either deliver a payload of toxins or molecules in to the cell by puncturing the exterior, or they simple create a pore in the membrane causing cellular depolarisation and death. As with phage and antibiotics however, these mechanisms can have resistance evolved against them.
As an additional point, unless you could somehow guarantee that the conjugations were sabotaged or ineffectual in some way, promoting conjugation artificially is almost certainly going to aid the spread of resistance and virulence determinants, actually worsening the situation.
3 A suicide plasmid
It is not trivial to 'confer significant advantages' on a cell. 225
Most plasmids are maintained by amelorating a significant disadvantage that is often supplied artificially, e.g. auxotrophy or antibiotic selection. Given the 'choice' bacteria tend to kick out the plasmids unless they simply cannot afford to live without it. Maintaining the replicon is an expensive process in terms of cellular metabolism and resource utilisation.
'In the wild' the weaponised plasmid would likely not persist long enough to be translocated in to any target of interest in a significant enough proportion to have a real effect. The key is that and of these ideas mentioned cannot simply kill a single target cell, as they will not have an appreciable effect on the population. The bacteria will recombine or straight up remove the plasmid if it's in any way deleterious or even neutral to them, until they've 'corrected' the problem.
Addiction modules and toxin-antitoxin systems are common to see in natural plasmids, as with the other ideas mentioned. Bacteria can recombine out the 'poison' though, and eventually over time lose the plasmids. If the toxin is encoded on the chromosome, it's a little more robust.
4 Bad plasmids
See addiction modules and toxin-antitoxin systems above.
I'm afraid in general I think you're underestimating evolution! 667