With deep sense of impartiality and ‘pure’ spirit of science, we must ask the fundamental question, who in our population likely to sponsor and or patronage the evolution of new pathogens from non-pathogenic microbes. The above question is not intended to kindle our though process or shape our thinking in any way towards how to eliminate the ‘sponsorship’ so that the worry about the pathogens we can banish but to bring a clear sense understanding for making future policies. Only then we can stop the possible emergence of the sister or brother or cousin of novel coronavirus in future.
Newer and newer species are likely to evolve in nature alongside the extinction of many. If the evolution is more compulsive among microbes means, the possibility of man missing such new microbes is quite high if they do not pose any new health rick to man. Some academic work may capture accidently some such new species, publish and there ends the interest and enthusiasm over the new species. The larger question for the debate is how a new species of microbe when emerge becomes human or animal or plant pathogen?
Parasitism is an opportunity by accident or conscious choice?
Do microbes evolve so naturally as saprophytic or parasitic?
If parasitic means, cognitively they evolve or just to fill a niche that is available, they evolve as a parasite? If to fill the niche means, then the new species cannot be fully qualified to be called as new evolution but only as a modified or re-adjusted variant or sub-species of some already existing microbe. If it had evolved as a parasite means, then we must ask whether it had evolved primarily as plant pathogen or animal pathogen where man is also an animal, in true sense, worst animal ever earth can have and nature can produce.
To become an animal parasite for a saprophytic microbe, the species required to transform from its dependence from the present trophic dependence level to totally different trophic level through the process of succession where the time frame of the microbe from strictly saprophytic to become an obligate anthropophilic parasite cannot be easily established or determined. The other question is whether any species refuse to become a parasite and adamant to remain as saprophyte?
The shift in the habitat or host preference is although linked strictly with ‘successes of the species but the opportunity also determines or influence such choice. From the perspective of a saprophyte having an opportunity to become a parasite is quite high because variety of vertebrate species the saprophyte might get to interact and learn about the new host is high and hence the familiarity and duration of such association may re-design the eco-genomics of the future generations of the organism is quite natural. Or else, the organism may develop newer skills to adapt in the new host. Keratinase enzyme production in zoonotic versus human pathogen has always shown quantitative and qualitative differences.
The question is why many saprophytes have not turned into parasite and why even an opportunistic parasite despite having abundant opportunity had not turned into a true pathogen?
Imagine, if a saprophyte wants to become a parasite from the evolutionary sense, still it is not that easy. It is not mere new learning of the microbe about the new host alone is sufficient to become a parasite, the organism also needs to equip itself several ways to become a parasite. No species on earth would want to shift from lazy, casual life to busy, hardworking life. Microbes are also no exception. Parasitic life means, in the battle field, kill and get killed, saprophytic life means, lazy, easy go life where toil is limited.
How microbes acquire the changes within that are required to live in the new host? When a new microbe invades man (totally a new species or the species that has never shown serious parasitism over man), the selection of the host cannot be based on the immunologically or chronologically weaker or aged host in the given population. The microbe is likely to invade its host at random based on exposure and frequency.
The immune competent host may evict the microbe and the weaker one would favour the organism by showing susceptibility which can be partial or full.
Partially susceptible host would favour the organism a chance to learn and gain more experience from the host and decide how live in the new host while the fully susceptible host may act as ‘mega’ laboratory for the organism to experiment and sharpen its virulence or traits either to over power or escape the immune surveillance. In both instance, the organism not only needs to learn about the host, also must develop its future progenies to competitively exist in human host.
Those who provide a bit of learning opportunity to the organism cannot be called as sponsor of the evolution of a microbe to become human pathogen but only those who provide laboratory facility to the microbe at no cost to the organism are only likely to make the organism highly virulent or obligate human pathogen.
Whenever there is a pandemic due to a new pathogen, the immune compromised and immune debilitated hosts either due to various co-morbidity conditions or due to chronological facts are the most fervent niche likely to make the new human invader a deadly pathogen.
If we allow the immune competent host to invade by the new pathogen, the possibility of the pathogen go fatigue and disinterested in the new host from the evolutionary perspective is quite high. No species ever wants its success at third or fourth attempt. When firs three or four attempts fail continuously and the host pose bigger threat to the invader, the invader withdrawing from the scene and limiting itself in some small pocket is high.
When we shut down the world and force people to follow social distancing especially when the pathogen has already invaded some immune compromised host, such measures are counterproductive and certainly bound to cause purulent effect in our society.
When we present ‘sandwich’ host system where one in every 1000 or more alone is highly susceptible means the probability of the new pathogen becoming a homicider is limited. The abundant resistance and small oasis ‘support situation’ in any new host system from the evolutionary perspective will not charm the new species. If we had protected the vulnerable group and allowed rest of the population to lead a normal life without any restriction and lockdown, by now the virus would have either disappeared or would have learned to live with us without inflicting much harm to man.
The chance of novel coronavirus become an opportunistic pathogen from its present status as secondary pathogen is also quite high if we had not imposed lockdown and other draconian measures.
Man is exposed to several plant pathogens every day. Large proportions of Indians are farmers and or engaged in allied occupations. Despite having such prolonged and sustained exposure of man to all those plant pathogens, none of them have become deadly to man so far. Although some of them are known to cause small health problems, either as opportunistic pathogens or by causing saprophytic infection (mycetoma, colonization of hair- Piedra etc). Very rarely a few may get infected terribly by those organisms but is not the norm.
Should we devise health security and other medical measures to all those people who may sponsor the evolution of new pathogens or worry about the pathogen? Evolution of new microbes, man may not able to stop. But those microbes becoming human pathogen can be minimized if we poke the new microbes with the ‘trick’ of Tenali Raman – a cat that doesn’t drink milk.
Any new species is if welcomed to its new world with hostility and challenges, the chance of the organism choosing the easiest and least resistant path to escape is high like how the electricity follows the path of least resistance.
Let us understand and accept the ‘sponsor pool’ that may favour and support the evolution of new pathogens and or a saprophyte to become a pathogen instead of creating hue and cry over the pathogen and destabilize economy and livelihood of millions in the name of saving them from the pathogen.
Written by Dr S Ranganathan.
Follow him @drsranganathan
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