We have modelled stress concentration around small gaps in anisotropic elastic sheets, corresponding to the peptidoglycan sacculus of bacterial cells, under loading corresponding to the effects of turgor pressure in rod-shaped bacteria. We find that under normal conditions the stress concentration is insufficient to mechanically rupture bacteria, even for gaps up to a micron in length. We then explored the effects of stress-dependent smart-autolysins, as hypothesised by Arthur L Koch. We show that the measured anisotropic elasticity of the PG sacculus can lead to stable circumferential propagation of small gaps in the sacculus. This is consistent with the recent observation of circumferential propagation of PG-associated MreB patches in rod-shaped bacteria. We also find a bistable regime of both circumferential and axial gap propagation, which agrees with behavior reported in cytoskeletal mutants of B. subtilis. We conclude that the elastic anisotropies of a bacterial sacculus, as characterised experimentally, may be relevant for maintaining rod-shaped bacterial growth.