The natural history of infection

Task : E. coli , bacterial resistance, plasmids, the nature of infection in vivo, legitimacy of bacterial identity.
The Natural History of Infection
Somewhere there’s the tale of the intrepid adventurer at the time they dug the Panama canal. As they dug, they dropped like flies, full of all manner of lurgy. Dysentery, Cholera, Typhoid, Yellow fever. Death was everywhere in this most unhealthy of environments and these poor white men just could not stand up to it. No resistance. Thousands succumbed. Of course the area was not new to humanity. By this time even the Spaniards had lived there for a good few years, with the West coast having been settled. This was of course, why they wanted the canal – to hasten the transport of goods to the far side of the isthmus rather than having to sail all the way around Cape Horn.
Anyway, as all these once strong labourers faded away and died our adventurer was unconvinced there was any intrinsic inability to fight off the infection. To prove his point he experimented on himself, drinking potions of infectious bacteria and he proved his point for he did not fall ill despite this challenge. Of course, he did not carry out any canal digging operations, remaining a mere bystander and “explorer”! Trouble was, of course, the labourers were worked to exhaustion, ill fed and probably malarial from mosquito bites. No wonder they were dying – the wonder was that any lived!
The story of these Spanish settlers is well told by Isabel Allende in Zorro in the era before the canal was dug, so it gives a base line scenario to work from. The idea of the baseline is such an important one in scientific endeavour. Without one you have to progress on assumptions which can so easily be incorrect or, even, warped. What do we use as the baseline in the discussion of infection and illness? How have we handled infection historically and what have been the outcomes?
By and large the matter only rises in historical discussion when speaking of mass illness. Plague, pestilence, cholera, epidemic, these kind of terms for terrible periods of population collapse. However there are also references to lepers in the bible and archaeologists often write of how such a skeleton must have died of some illness or other damage they cunningly deduce.
So I am fairly sure that there has always been a loss of life resultant from bacterial, fungal, protozoan and worm infestation. There would have been not infrequent periods of semi-starvation, inadequate shelter, thirst and consumption of unclean food and water. Further there would have been injury leading to infection.
As this was part of life and living so our bodies were accustomed to it. Our blood borne immune system, primed by early breast feeding as well as contact with ambient micro-organisms would have been oft called on in homeostatic manner though probably rarely to fight off full blooded infection. However it seems probable that there was quite high childhood mortality, for a range of reasons, mostly starvation and accidents one would imagine. Yes, sabre toothed tigers, that sort of thing!
Being settled, in communities, is so recent in human history that the health benefits and disbenefits are not yet clearly defined. Mass infection seems to have arrived resultant on this mode of living but probably dependent on dietary deficiencies and other social and housing type issues. Witness biblical Egypt at the time of Moses and, much later, the Great Plague in England. In fiction there is Marquez’ “Love in the time of cholera” to show had infectious disease follows poverty and deprivation.
Today’s societal defence is two pronged – antibiotics and vaccinations. The cosh and the crutch approach. Both derive from apprehension and panic and both still are driven in that manner. Antibiotics, antibacterial chemicals, can still be effective in combating severe bacterial infestation, in situations where the body’s internal defences have proved inadequate or have been otherwise compromised.
How and why this happens is a moot point. Certainly Marquez’ description is still relevant but a range of corporal and mental stresses can induce susceptibility. Maybe some infections are just damn unpleasant and “out to get us” but I find it hard to go with that. I find them more as a constant challenge to our fitness, our cohesion, our integral preparedness. Thus, if you maintain your corporal and physiological integrity, you are protected against such outcomes.
This works far less well for protozoans and the impact of malarial mosquitoes for which I am not sure we have yet developed a clear picture of the human ecology which leads to these problems. Certainly the anti-bacterial immune-memory system provides a model for clear population preparedness plus an inherent adaptability innate to all of us. This seems lacking with respect to eukaryotic invaders. Maybe sickle cell is an indication of there having been a range of local adaptations which we are now so not aware of and seriously lacking in availability. Simply, we have moved around too much and any genetic adaptations to combat other protozoans are lost in transit. They may even be the basis of perceived genetic disorders these days, much as SCA is problematic away from mosquito land.
I don’t buy this constant war twixt humanity and the bacterial world, as I suggested above, but I do accept that in a situation where initial defences have been bypassed and life is threatened antibiotic medications can be vital. Everyone knows how they have been overused, however, and how bacterial mechanisms to resist these chemicals have developed. This reaction both questions the nature of bacteria and demonstrates the tenacity of life.
Far from being clearly separate entities it can be shown that nominally different species of bacteria can exchange the genetic information needed for antibiotic resistance. Further these factors are shown to be carried on a separate genetic parcels, named plasmids. In contrast to the full bacterial genetic code, these tiny rings contain maybe two to ten genes. They can be passed on in a very short time. Well the whole genetic material can be copied across in half an hour at cell division so this is a minute or two.
Some times not all the information will cross but at others there can be accumulation of resistance genes where several resistances are brought together. In a very few years there have developed plasmids encoding multiple resistance which are transferable at will between all infective bacteria. Thus there exist MRSA, multiply resistant streptococcus aurea.
This proliferation of resistance has been driven by one organism – ourselves. In two prime, selective locations we select for the development of resistance by massive use of the antibiotic chemicals which obliterate those bacteria not carrying resistance. Obviously hospitals and scenes of medical practice is one such location but the other is the livestock farm.
Crassly in farms antibiotics are used both in treatment of illness but also prophylactically. Chicken grow faster when fed antibiotics, for example, and dairy herds are quite heavily medicated. Unsurprisingly much produce of modern farming contains both antibiotics and, if you are unlucky, antibiotic resistant bacteria. These are part of the constant resupply of hospitals with resistance plasmids.
Very promiscuous, I usually say, and with such ready cross transfer of information, it is quite hard to differentiate between different bacterial types. They are a perpetually changing, a drift of genotypes and our resistance to their harming us relies on our own constant updates. I hold that is the norm and that our systems are wholly accustomed to this function.
Childhood infections? Flu? Both scenarios seem to be representations of the basics outlined above. In childhood whether there is an inability to fully function until such infection has been worked through is a useful conjecture but hard to back up scientifically. The body does seem, however, to gain extra strength following such an event.

This is a draft document and will be edited/progressed.

About greencentre

Non grant supported hence independent scientist, green activist, writer and forest planter.
This entry was posted in Ecology of disease, Uncategorized. Bookmark the permalink.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s