toxicology - Why are bacteria immune to snake poisons?

In a test I was asked why bacteria are insensitive to snake toxins.

Is it their membrane that provides a barrier to the toxins? Or do snake poisons have specific targets and thus cannot bind to bacteria?

Answer

Short answer
Many snake poisons target specific proteins not present in unicellular organisms.

Background
The question is admittedly broad but the idea behind this question is pretty much what you indicate in your post - many venoms target specific proteins and do not simply destroy their target by, e.g., disrupting gross cellular structure (like alcohol does for example). Instead, they target specific molecules that are essential for the survival of their prey.

Snake toxins can be categorized according to the organ systems they target, namely :

• the central nervous system


• the cardiovascular system


• the muscular system


• the vascular system

Central nervous system toxins are carried by elapid snakes like cobras, kraits and the taipan. Typical targets are the nicotinic acetylcholine receptor and the muscarinic acetylcholine receptor. Blockade of these receptors at the neuromuscular junctions resulting in death by asphyxiation. Acetylcholine receptors are not present in bacteria.

Cardiovascular toxins are pretty diverse and include things like angiotensin-converting enzyme inhibitors (leading to a drop in blood pressure) and glycosaminoglycans (the sulphated carbohydrate moieties that occur abundantly in cells of cardiovascular tissues) binding proteins that lead to cardiotoxicity. Again, the targets are specific molecules involved in heart function and hormones, stuff not present in bacteria.

Muscular toxins include those that bind specifically to the sarcoplasmic reticulum of muscles or interfere with specific second messenger systems messing up muscular function. Again, quite specific targets not present in bacteria.

Lastly, typical vascular system toxins include anti-coagulants such as protein C activators and inhibitors of prothrombin complex formation. Again, specific targets.

Reference
Koh et al., Cell. Mol. Life Sci (2006); 63: 3030–3041