Why don't bacterial cell walls prevent bursting when attacked by the complement?
Although this seems to be a simple question on the exterior, the answer is going to be confusing and unclear because we still don't know the answer exactly. 

Short answer - MACs are bactericidal not because of water gushing in. It is due to other mechanisms effected by damage to membrane integrity.

Long answer 

First of all, I am assuming you already know the complement cascade, the pathways and the like, and I won't get into it. But to mention in passing, MAC is not the only way the complement can help the immune system. It can also opsonise antigens and release anaphylotoxins to modify the immune response.

Most studies concerning the assembly of the MAC and the resulting membrane lesions have been conducted in model systems, e.g. erythrocytes and artificial lipid bilayers. The advantage of these systems is the ease of characterizing the membrane lesions compared to bacterial membranes. Also, complement fixation tests (which use erythrocytes and complement) have been widely used even diagnostically until not very long ago. The osmotic damage, ion effluxes that you talk of happen here and leads to the lysis of erythrocytes. Even in their case, there are 2 models of how MACs work - one is by making a pore (in the pic) and the other is by forming leaky patches in the membrane. However, the way bactericidal MACs work is thought to be different and a little more complex than this - 



This picture may have been used for just didactic purposes but cannot be applied in a bacterial system simply because bacterial cell envelopes are different. The two major groups - Gram positive and Gram negative cell walls are important to differentiate while discussing the mechanism of MAC bactericidality. It is important to note that MAC mediated bactericidal action has been reported predominantly only in Gram negative organisms. This resistance in Gram positives is thought to be not because of the osmotic turgor or turgidity but because of the thick peptidoglycan in Gram positive bacteria, preventing access to the inner cell membrane where the MAC assembles. There are MAC resistant Gram negative bacteria too, but let's not discuss that here. It is not off-track to mention here that species like Neisseria where the capsule is thin and the peptidoglycan is too, are more susceptible to complement damage.

So, assuring that the MAC mediated bacterial lysis is not just water gushing in, how is it thought to happen??

For this, we need to revisit the structure of the Gram negative cell wall. The cell wall structure is quite intriguing since there happen to be two lipid membranes enclosing a periplasmic space which contains little peptidoglycan that Gram positives have much more.



Since there are two lipid membranes, technically, there's a possibility that the MAC can be formed on both these layers (MAC's assemble on hydrophobic membranes). MACs assembling on the OML (outer membrane layer) are not sufficient to cause lysis. It is confirmed that the damage has to occur to the IML (inner membrane layer). Inner membrane damage is thought to be bactericidal since it is more restrictive in its permeability than the OML. Also, the IML is linked to several important cellular, metabolic functions that require proper ionic gradients. One example is the oxidative phosphorylation that takes place around the IML.

This should answer your question in that the mechanisms of cell lysis seem to be slightly different in bacteria than the model systems (erythrocytes), but let us delve a little deeper into this.

One persistent question is "how can something as huge as the MAC, penetrate the OML and the peptidoglycan layer, to reach the IML to cause damage?" The hypotheses that MAC just forms a hole in the OML and other serum factors seep in and cause damage to the IML has been ruled out since complement alone can be bactericidal in nature. To explain this, two models have been proposed - 

One, where the complement attaches at special sites in the membrane where both OML and IML approximate (at special sites where large proteins span both membranes) and another where, the complement creates a pore to allow C9 monomers to leak in, in turn polymerizing to damage the IML.

I assume this explains it all. Still, I implore you to refer to the link below and correct me if I've been wrong anywhere. 


  Reference : The bactericidal mechanism of the complement membrane attack complex, Lars Ootes, (PDF)