Quizzing the Anonymous - Why do bacteria kill?
Why do bacteria kill?|
Pathogenic bacteria often kill by producing toxins, some of which are the most lethal poisons known. But what is the goal of killing one's own host? Why do the bacteria produce these toxins? The textbooks, after going into the excrutiating details of the action of cytotoxins, typically end on a philosophical note:
...why certain bacteria produce such potent toxins is mysterious. The production of a toxin may play a role in adapting a bacterium to a particular niche, but it is not essential to the viability of the organism. Most toxigenic bacteria are free-living in nature and in associations with humans in a form which is phenotypically identical to the toxigenic strain but lacking the ability to produce the toxin. http://www.textbookofbacteriology.net/proteintoxins.html
a quick review of the action of toxins is here http://www.cdc.gov/ncidod/eid/vol5no2/schmitt.htm
I've just read an article that suggests, without providing much detail, an interesting idea, which is new to me:
The toxins are not aiming at the host but rather at the competition: the inflammation creates the conditions when benign bacteria cannot survive providing the lethal bacteria with their only opportunity to spread. So the cholerae vibrio induce diarrhea not to spread (as I've been told when I was a student), as they will get into water anyway, but to flush the intestines of the benign gut bacteria that get in the way and even help the body to get rid of the invasive guests. The need to kill the fellow bugs is so great, as these are super sturdy, and it requires such extraodinary means that sometimes the host simply gets in a way; it is just too weak. Our immune system is seldom the problem for bacterial proliferation: our own cells are greatly outnumbered by the bacterial ones. The other microorganisms may be the problem.
Come to think of it, there could be something to this idea, but it does not have to be limited to other bacteria. Take botulism, for example: C. botulinum are anaerobic soil bacteria that have no intention of living in a human. Why is it producing neurotoxins? The toxin targets SNARE proteins that regulate vesicle fusion (taking transport vesicles across the membranes) with some of these vesicles (in motor neurons) having neurotransmitters. This type of protein is also involved in the absoprtive feeding in soil fungi
Perhaps it is another case of getting in a way. The bacteria seek to kill yeasts in the soil that are feeding on them. But we (metazoa) have the misfortune of sharing with our fungi sisters the opishtokont ancestry that includes the particular design of SNARE proteins. The two SNAREs are pretty close despite 900 Myr of divergent evolution
The bacteria try to stunt the growth of its mortal enemy and accidentally kill the harmless weakling that crosses their path?
This is so unfair. We are not even important enough to be wanted dead...
Why do bacteria kill?
Why don't those soil fungi colonize us and feed on our gut bacteria?
Fungi are "enemies" of the soil bacteria not because they eat them, but because they inadvertantly kill them; they compete for the same food: decaying organic matter. Fungi secrete their digestive enzymes and then absorb small molecular fragments. These enzymes kill soil bacteria, so they strike back. The fungi strike back with antibiotics, and so this warfare goes on.
Soil fungi had long colonized the gut, but mainly in the herbivores. The problem is low oxygen concentration, so these are very special anaerobic fungi. The objective is not dwelling in the gut. The objective is to have the heyday once pooped out (all this food!): they found the perfect place to disperse their spores. It is part of their life cycle. Gut bacteria are of no interest to them.
|Date:||January 29th, 2010 05:59 am (UTC)|| |
You mean, we picked the wrong bacteria do be symbiont with? The weak ones???!!
No, WE are the weaklings. They can cope with us. They can't cope with each other.
|Date:||January 29th, 2010 11:21 pm (UTC)|| |
That I understand. The question is: why did we pick a weaker bacteria as a symbiont? Why don't we cooperate with the ones capable of dealing with any intruder quickly and decisively?
I think it may be impossible to be this tough and still having an alive host. The pathogens do unbeliveably clever tricks to subvert the body. Like meningitis that secretes proteases that destroy IgA antibodies. They are high-stakes players willing to risk it all on setting a foothold in the body. The symbionts are not willing to takes such odds. They can squeeze the other bugs out but they would not cross a certain line because they already have a host that tolerates them. When they cross this line, like E coli O157, they become pathogens themselves. This one also causes diarrhea to get rid of the competition.
|Date:||January 29th, 2010 09:31 am (UTC)|| |
I've been thinking about the same question... It's nice to hear some ideas, thanks. I wonder if it also works for tetanus.
I do not know about tetanus, but Finlay gives another interesting example: mouse analog of typhoid Salmonella. If you give a mouse tons of antibiotics, wait a little, and then infect it with Salmonella, it is just upset stomach. But if you infect a mouse without this pre-treatment, it is a full blown typhoid-like disaster that can easily kill. Finlay tells that the pathogen is driven to invade gut lining tissues to escape the competition in the gut. If there is no competition, it remains in the gut without causing trouble. Its cytolethal distending toxin is pure genius: somehow I missed on CDTs. It breaks double-stranded DNA provoking massive damage-response from the host cell that activates its apoptosis. The bacterium also injects flagellin into macrophages, to the same effect (it somehow induces tumor necrosis factor). This thing knows what it is doing.
|Date:||January 29th, 2010 08:27 pm (UTC)|| |
Why do bacteria kill?
I think death of the host could be advantageous from evolutionary standpoint in some circumstances because it could help to spread bacteria to other hosts. Being killed by bacteria, the host could be eaten by other carnivore which becomes the new host and so on. Important feature is that the same bacteria could kill one host but not an another; this feature could help to ferry bacteria on a long distance seeding their colonies through food chain infections from one type of host to another, through carnivore-herbivore cycle and so on.
That's imaginative thinking, but the problem is that there is not too much of a chance for the bacteria to spread from the carnivores back to the herbivores. Furthermore, there are too few carnivores to make this scheme of proliferation running. Furthermore, carnivores produce strong septic antitoxins because they consume carrion. I, actually, think you are incorrect. There is no decisive advantage in killing the host. Just as they say, for every bacterium that makes toxins you can find a cousin that does not and seemingly does just as well. There are also some bacteria, like Y. pestis that causes plague that is too clever for its own good, as is uses macrophages to ride into the lymph nodes where it multiplies. It destroys the immune system too efficiently, a bit like HIV, causing the complete havoc. Toxins is just one way to kill a human...
|Date:||January 30th, 2010 12:25 am (UTC)|| |
I, actually, think you are incorrect.
I don't persist, that's just a hypothesis and that could be not common, just one kind of diversity of evolutionary strategies, other species cold utilize other ways to survive. But we must assume that if bacteria kill there should be two possibilities
- It is somehow advantageous for them
- It is inadvertent "back-fire" of a kind of different adaptation feature, which is advantageous in their usual habitat, but makes devastating and self-destructive effect being put in this particular conditions, when bacterium appear inside hosts, which is actually unusual for them in general.
Your instance with botulinus at my point of view is a sample of the second case. But if this is a common way for most bacteria producing toxins, we have to observe their normal habitat outside hosts in wild exactly as it appears with botulinus. I'm not a microbiologist so I don't know if its true. Could you confirm or disove that?
|Date:||January 30th, 2010 12:30 am (UTC)|| |
I mean we must observe not only harmless cousins but the very same bacteria producing toxin existing in wild outside hosts and this toxin should be essential for it to survive.
No, generally this would not be correct. Many pathogens simply do not occur in the wild, they are always parasitic; also the use of neurotoxins is a great rarity. Extreme virulence IS disadvantageous as far as the exploitation of the host is concerned. But this is not the only concern. Other bacteria are the concern and other strains are also the concern. As I wrote, there is no good, accepted, proven explanation how virulence evolves. Usually, you are treated to a classical story: there are several strains and the heat of the competition between the strains leads to overexploitation of the host; they get carried away with beating each other to the finish line. The worst situation is when the bacteria are closely related because then they grasp for any advantage even if it makes no sense in a long run. Here is the typical take:Competition among different parasite genotypes within a host is predicted to affect virulence. The direction of this effect, however, depends critically on the mechanisms that parasites use to compete or to cooperate with each other. One mechanism that bacteria use to compete with each other is via the production of bacteria-killing toxins. This warfare among parasites within a host is predicted to reduce the rate of host exploitation, resulting in lower virulence. By contrast, if parasites within a host are highly related, there could be a reduction in within-host conflict, increasing virulence. We examined this idea by allowing an insect-parasitic nematode (Steinernema carpocapsae) and its symbiotic bacteria (Xenorhabdus nematophila) to evolve for 20 passages under two different migration treatments (low and high). We found that host mortality rates were higher in the low-migration treatment when compared with the high-migration treatment. In addition, bacteria isolated from the same insect host inhibited each other's growth, but only in the high-migration treatment. These results show that population structure and interactions among parasites within hosts can be critical to understanding virulence.http://www3.interscience.wiley.com/journal/120755761/abstract?CRETRY=1&SRETRY=0
The idea is that extreme virulence is a competition driven to such a gear when the survival of the host becomes a secondary concern. This is not necessarily the case, but that's what you'd be told. Parasitic bacteria are stupid. They do not think strategically. All they really want to do is outdoing their own kin. Exploiting you are just the means to this goal, and you can become the collateral damage. But killing you on purpose serves no goal at all.