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Spatiotemporal evaporating droplet dynamics on fomites enhances long term bacterial pathogenesis

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Naturally drying bacterial droplets on inanimate surfaces representing fomites are the most consequential mode for transmitting infection through oro-fecal route. Saptarshi Basu discusses a multiscale holistic approach to understand flow dynamics induced bacterial pattern formation on fomites leading to pathogenesis.

Image courtesy of interviewee. February 29, 2024

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This video video discusses research conducted during the COVID-19 pandemic focused on how diseases, particularly caused by bacteria and viruses, are transmitted. It begins by explaining the mechanisms of virus transmission through respiratory droplets and surfaces, leading to the exploration of bacterial transmission in a similar manner.

The researchers aimed to understand how bacteria proliferate and spread when they settle on surfaces, known as fomites, which can harbor pathogens and act as incubators. The study highlights the importance of inanimate objects such as doorknobs, computer screens, and other surfaces in the transmission of diseases, particularly in relation to antimicrobial-resistant bacteria.

The research focused on various bacteria, including Salmonella typhi and other "escape pathogens," examining how they survive under different conditions, including desiccation (drying out) and nutrient availability. They used different physiological mediums to simulate droplet dispersion and observed how the drying process affects bacterial viability and virulence.

Key findings include that while many bacteria die when dried, those that survive tend to become more virulent. Furthermore, the bacteria's location within droplets influences their survival due to resource-sharing dynamics. The study underscores the impact of environmental factors—like humidity and temperature—on bacterial survivability and potential health risks, suggesting that certain geographical contexts could lead to higher transmission rates of bacteria. The research highlights the complex interactions between physical conditions and biological responses, emphasizing the need for understanding these factors for better preventive measures against bacterial infections.

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X-TIMESTAMP-MAP:LOCAL=00:00:00.000,MPEGTS=900000

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What happened was that during this covid period,

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we started doing a lot of work

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on disease transmission, so to say.

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So, with disease transmission, we did a lot

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of work on viruses.

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So how virus actually spreads through the droplets

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that is respiratory fluids, mainly, either

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through the aerosol groups

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or it, if it settles on the surface,

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it forms this small patches, and then you touch it

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and you, you touch anywhere in your

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mouth and you get infected.

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So these were the reported, you know, ways

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by which Covid was supposed to infect us.

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As a result of that,

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after the covid was over, we thought

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that why not take the same methodology

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and now take it to bacteria

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because bacterias are easier to handle

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because, you don't need a BS O three type of facility,

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which is biosafety level three.

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You can still work with bacteria in a lab setting

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with certain safety measures,

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and you can try to see that

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how the bacterias actually proliferate, how do they infect

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and how do they transmit, when you,

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when it actually settles on the surface.

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So, so

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that was the context in which we started looking at this

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line of work, which involved bacteria.

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So the fomites are basically any surfaces,

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so any inanimate surfaces.

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So it can be like your, you know, the, the computer screen,

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it can be the table, it can be the doorknob of your door

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that is behind you.

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It can be basically the buses, it could be the seed,

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it could be the Amazon packages that you have,

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even it could be vegetables, it could be anything.

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So, so strictly these are inanimate objects, so to say.

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So what happens is that these,

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surfaces can actually harbor, these pathogens.

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So they act as some kind of an incubator

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for these pathogens.

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So, unlikely

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because you normally would try to believe that, okay,

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these things looks very benign, okay?

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Because these are day-to-day objects.

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But what happens is

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that the bacterias do not die when they settle on these

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surfaces and they don't die.

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So they actually are alive.

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And by the time when you touch these surfaces

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and then you touch anywhere in your mouth

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or wherever, all these orifices

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that we have, it gets transmitted.

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There is a potential

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that it can get transmitted into your body,

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and this can cause you, diseases of all kinds.

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Now, we did not just deal with salmon ever typhi.

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We also, this is the most virent gut pathogen, by the way.

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So it is a pathogen of the gut,

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but there are other escape pathogens,

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that we have also studied in the same,

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it's called escape pathogens,

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which includes flip shalia pneumonia, then pseudomona, staph

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staph bacteria, the phi opus orus.

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And there are a whole lot of these bacterias,

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which mainly contribute to this antimicrobial resistance

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that we see these days.

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So these are deadly pathogens.

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They account for quite a bit of death,

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especially in the third world countries also.

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So, so, so this is, this is something,

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this is antimicrobial resistance as a, as a result of that,

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it is important to study that how this bacteria spread

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and how the virulence is actually affected so

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that you know exactly what to do, how

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to do the preventive measures.

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So this basically triggered the

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whole, you know, the process.

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We started with salmonella typhi,

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but then we did all other escape

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pathogens as well in due force.

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I mean, these are subsequent works after we, we did this.

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So that was the most logical thing when you sweat

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or when you cough,

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or when you are, when your human excreta, okay,

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it a pipe bursts.

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And so there are droplets everywhere.

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So you know, these small, liquid, vessels basically,

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which contains this bacteria.

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So they are spread all over.

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Now, one methodology is

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that you ingest the droplets directly, which happened,

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much during the covid and as well as in pneumonia

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and other kind of diseases.

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But there is lot of cases

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where it actually settles on the surfaces around you.

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So in order to mimic that, what we did is that we,

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we actually had this droplets of different types of fluids.

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So the three different types of fluids

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that were there in this work is seline, which is basically,

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salt water,

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and then of course you have dextrose and new seed.

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So the rational behind is

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that seline is your respiratory fluid.

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So it is mostly of seline new seed is a gastro fluid.

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So your gastro gastrointestinal system has got mu C

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and so dextrose in a very similar wave, right?

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So these are fluids which are commonly, you know,

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common physiological mediums in which the bacterias

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basically get nurtured.

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So you make droplets out of this, okay?

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I mean, droplets of a particular volume.

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And then we deploy it on different surfaces.

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So this could be steamed wood, you know, tomato skin,

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cucumber skin, anywhere and everywhere, right?

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And then we allow it to dry under different temperature

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and relative humidity conditions.

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So that means the high low temperature,

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high relative humidity, low relative humidity.

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Then we use a series of diagnostic techniques,

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which includes mi microparticle image velocity entry,

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basically to measure the flow field inside those droplets

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as these droplets are basically dry,

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because as, as you dispense these droplets on the surface,

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they dry over a period of time that is natural.

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I mean, everything evaporates.

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So as they dry, they create a flow field inside the droplet,

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this tiny droplets

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that you have less than a millimeter size.

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So these bacterias then get churned inside those droplets,

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and as they get churn inside those droplets,

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they form these very spectacular patterns.

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Some of these things were reported in that paper as well.

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So they form these spectacular patterns,

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and depending on the physiological medium that you, it's,

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or seline or, you know, dextrose,

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these patterns actually varies.

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So they, they,

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they show the spectacular variation in patterns.

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So what we do is that

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after everything is dried off, we, we photograph everything.

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Then we take it for

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what we call scanning electron microscopy.

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And we do, you know, atomic force microscopy as well

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as normal fluoresce imaging, which is confocal imaging.

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We try to see that where these bacterias are,

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what planes they are located,

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and what is a topography of the deposit,

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and how the deposit basically looks like,

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because these are very tiny,

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you cannot see them with your naked eyes.

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Once all these things are done, then we take these deposits.

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Now we red dissolve them,

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and we put it in what we call a cytosis type of a project.

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Uh, firstly study the viability that how many

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bacterias which were there originally in the droplet,

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how many of them actually survive

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after the precipitate forms?

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So that is a viability count.

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So you will find that most of the bacterias actually die.

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I mean, significant percentage actually dies

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over a period of time.

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Then we dissolve this, you know, this precipitates,

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and then we put it in our phagocytosis process,

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which is a standard immune process that you try to check,

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to see that how many of these, what is a ulence level

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of these bacterias?

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So there we found that the bacterias are very virulent,

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so whichever ones survive,

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they become more virulent than the ones

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that were not in the form.

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So that was spectacular.

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So I mean, so it's almost like this,

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that if you have a hundred bacterias,

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normally this a hundred bacterias would be viable under

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normal conditions, but movement, the form of fomite,

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that means they get dried out of this a hundred,

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maybe 10 bacterias actually survive,

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but those 10 have the ence of mold like 30.

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So that is to give up, I mean, very, you know, global kind

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of a viewpoint.

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Uh, so then we also do, we also did in vivo experiments,

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which is basically to feed this precipitates to mouse mice.

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And we found that the same results actually holds,

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that means the bacterias becomes more virulent,

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but many of them actually die in the process.

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So it's almost like a mini survival of the fittest

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that is going on, that that means most of the bacterias die,

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but whichever does not die.

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They know that, okay, these are the kind

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of stress conditions we have felt, and

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therefore we need to be more, more agile, so

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to say, to survive.

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So that makes them more, you know, dangerous to mankind.

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I mean, for the, for the, for animal infections.

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So that is an interesting question,

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but that goes more into the physics of the problem.

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See, that means when this drop, that's actually dry, okay,

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that precipitate is not a homogenous precipitate anymore

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because there is something called

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what we call the coffee strain effect.

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So that means as the droplet EVAs,

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there is an outward flow towards the edge of the droplet,

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which transports most of the bacterias to the edge, right?

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But some bacterias also remains at the center.

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So what we found is that, just to give a cut,

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a long story short, the bacterias, which are at the edge

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are more, they survive more than the bacterias at the center

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because they kind of, they're close together.

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So it must be, there is some sharing of resources

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that happens and some kind of a stress relieving mechanism

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that they do, which makes them survive.

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Uh, I mean, the viability part in those bacterias are more

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than the bacterias at the center.

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So it is not just one size fits all, even in

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that small droplet, even in a spatial sense,

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the central deposit actually has got less viable bacterias

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compared to the deposits of the edge.

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So, but obviously,

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that goes into the nitty of the details.

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That's why you need to study what it is.

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And also, another thing we found that, you know,

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when you have new scene,

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mu scene is a very sticky substance.

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This is what, when you cough, this is the, the, the flame

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that comes out of your mouth.

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So that is basically new scene.

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So mucin actually sometimes forms a protective sheet

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around the bacteria.

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It's like a c**n kind of a thing.

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So it protects the bacteria from this, mechanical

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and osmotic stress

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and desiccation stress that we call it desiccation stress,

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is that when you dry something, it gets desiccated,

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the water actually leaves as a result of that.

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Like, we can get dehydrated.

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So that will be like a desiccation process.

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So the bacteria happens the same way.

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So this forms a sheep

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and somehow protects the, you know, the hydration level

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of the bacteria in a very micro sense.

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So you always see that when you use mucin compared

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to seline, bacteria survive more in mu than in seline,

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because mu seen A is a nutrient rich medium,

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and b, it perhaps forms this protective sheath

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around the bacteria protecting it from the harsh

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environment that we see around.

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So for the bacteria, it's a harsh environment, so

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that gives it more longevity, so to say.

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I mean, so that, that, so the topography

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therefore becomes very important, not just from a,

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not just from a system point of view,

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but also to understand what is exactly going on.

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So here is a very typical example in which you see fluid

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mechanics, which is basically your osmotic stress,

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dessication stress, and your mechanical stress

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and the flow, they actually alter the bacterial viability

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and virulence, which is entirely a biological phenomenon.

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This is basically how the bacteria sees a threat

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and how it regulates, its metabolic rate,

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its genes and all those things.

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But the response function is something

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that you encounter in everyday life.

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It is like, it is the same fluid mechanics

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as we throw a stone or, you know, you know, flow

11:47.975 --> 11:51.935
through a pipe, but that influences the bacterial,

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longevity and the bacterial.

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So I thought this was a spectacular merging of two fields.

11:57.625 --> 12:00.725
If you call it like the, the macroscopic fluid mechanics

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and the microscopic, biochemistry

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or microbiology, if you call it, they kind of meet together

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and they give you the spectacular, spectacular outcome,

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the bacterias, okay?

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Always when they are desiccated.

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And our subsequent works also show the same thing,

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that if they are desiccated fast,

12:20.675 --> 12:23.725
that means if you are in a hostile environment

12:23.835 --> 12:26.965
with low relative humidity versus an environment

12:26.965 --> 12:28.725
where the relative humidity is kind

12:28.725 --> 12:30.805
of a little bit on the higher side,

12:30.835 --> 12:33.405
that means it's a slow vaporization process.

12:34.025 --> 12:35.125
The bacterias tend

12:35.125 --> 12:38.525
to survive more in the higher relative humidity settings.

12:38.555 --> 12:40.565
That means when it is nice

12:40.745 --> 12:42.925
and easy, that means it's using water,

12:43.385 --> 12:47.445
but it has enough time to kind of adjust itself to it.

12:47.985 --> 12:51.245
So that is one thing that means, droplet,

12:51.245 --> 12:52.325
which is evaporating

12:52.345 --> 12:55.165
or a bacteria containing droplet sitting on a surface,

12:55.215 --> 12:59.325
which is evaporating in Africa versus in,

12:59.395 --> 13:03.245
very humid conditions like, like India, some parts of India,

13:03.245 --> 13:04.405
especially in the coastal areas.

13:04.945 --> 13:07.725
So they will have different levels of survivability

13:08.145 --> 13:11.805
or viability for the exact same bacterial concentration,

13:12.115 --> 13:13.805
same bacterial strain, everything.

13:14.105 --> 13:16.725
So that is, that is kind of remarkable to begin with.

13:17.065 --> 13:19.085
So that matters. So the weather conditions.

13:19.085 --> 13:21.085
So one way of saying this is the weather condition

13:21.085 --> 13:22.445
matters a lot.

13:22.455 --> 13:25.165
Covid has taught us that yes, it matters bacteria,

13:25.755 --> 13:28.285
that this, this kind of studies also shows that it matters.

13:28.625 --> 13:30.645
The other part is that depending on

13:30.655 --> 13:32.485
where the bacteria is residing,

13:32.485 --> 13:34.285
that means whether it is a gastro fluid

13:34.585 --> 13:36.325
or whether it is coming from your mouth

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or from other parts of your body

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that determines its survivability as well,

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because of the reasons that I mentioned that, you know,

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forming the sheath and all this, all this, all this stuff.

13:47.065 --> 13:50.125
So that chemical composition of the medium also matters

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as much as the desiccation stress

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and the fluid mechanics of the problem, as well

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as the weather conditions.

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So all this matters.

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So I would say even a bacteria, for example,

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in a coastal region, same type

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of bacteria in a postal region, identical conditions

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otherwise would actually be more viable

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and more destructive than the bacteria in some other area.

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I mean, this is the first, first cut evidence.

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I mean, this is the point at which it enters the body.

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After that, of course, our immune

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system actually takes over.

14:21.735 --> 14:24.915
So it depends on the demographics also that some parts

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of the, you know, some parts of the world,

14:27.075 --> 14:30.155
some people are better equipped to handle a disease compared

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to some other part that is our then our adaptive

14:32.895 --> 14:34.795
and innate immunities actually kicking.

14:35.175 --> 14:37.995
But from a transmission point of view, the dosage

14:37.995 --> 14:40.915
that is entering into your body, that would be higher

14:42.775 --> 14:45.615
compared, and that is determined by the weather conditions,

14:46.335 --> 14:48.695
chemical stressors, and the mechanical

14:49.015 --> 14:50.815
stresses. So after that,

14:50.815 --> 14:53.185
What happens is like your, your anatomic

14:53.205 --> 14:54.865
and your physiology then takes over,

14:55.365 --> 14:58.265
and, that is for the doctors to determine exactly

14:58.485 --> 15:00.705
how the proliferation happens after that.

15:00.845 --> 15:02.945
But we have seen in our cell lines

15:03.005 --> 15:06.185
and individual experiments that that is exactly the case.

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This should translate into higher, you know,

15:09.405 --> 15:11.585
higher disease comes, so to say.

00:00 - What happened was that during this covid period, we started doing a lot of work on disease transmission, so to say. So, with disease transmission, we did a lot of work on viruses. So how virus actually spreads through the droplets

00:13 - that is respiratory fluids, mainly, either through the aerosol groups or it, if it settles on the surface, it forms this small patches, and then you touch it and you, you touch anywhere in your mouth and you get infected. So these were the reported, you know, ways by which Covid was supposed to infect us. As a result of that, after the covid was over, we thought

00:36 - that why not take the same methodology and now take it to bacteria because bacterias are easier to handle because, you don't need a BS O three type of facility, which is biosafety level three. You can still work with bacteria in a lab setting with certain safety measures, and you can try to see that how the bacterias actually proliferate, how do they infect and how do they transmit, when you,

01:01 - when it actually settles on the surface. So, so that was the context in which we started looking at this line of work, which involved bacteria. So the fomites are basically any surfaces, so any inanimate surfaces. So it can be like your, you know, the, the computer screen, it can be the table, it can be the doorknob of your door that is behind you. It can be basically the buses, it could be the seed,

01:29 - it could be the Amazon packages that you have, even it could be vegetables, it could be anything. So, so strictly these are inanimate objects, so to say. So what happens is that these, surfaces can actually harbor, these pathogens. So they act as some kind of an incubator for these pathogens. So, unlikely because you normally would try to believe that, okay, these things looks very benign, okay?

01:56 - Because these are day-to-day objects. But what happens is that the bacterias do not die when they settle on these surfaces and they don't die. So they actually are alive. And by the time when you touch these surfaces and then you touch anywhere in your mouth or wherever, all these orifices that we have, it gets transmitted. There is a potential

02:16 - that it can get transmitted into your body, and this can cause you, diseases of all kinds. Now, we did not just deal with salmon ever typhi. We also, this is the most virent gut pathogen, by the way. So it is a pathogen of the gut, but there are other escape pathogens, that we have also studied in the same, it's called escape pathogens, which includes flip shalia pneumonia, then pseudomona, staph staph bacteria, the phi opus orus.

02:47 - And there are a whole lot of these bacterias, which mainly contribute to this antimicrobial resistance that we see these days. So these are deadly pathogens. They account for quite a bit of death, especially in the third world countries also. So, so, so this is, this is something, this is antimicrobial resistance as a, as a result of that, it is important to study that how this bacteria spread and how the virulence is actually affected so

03:15 - that you know exactly what to do, how to do the preventive measures. So this basically triggered the whole, you know, the process. We started with salmonella typhi, but then we did all other escape pathogens as well in due force. I mean, these are subsequent works after we, we did this. So that was the most logical thing when you sweat or when you cough,

03:36 - or when you are, when your human excreta, okay, it a pipe bursts. And so there are droplets everywhere. So you know, these small, liquid, vessels basically, which contains this bacteria. So they are spread all over. Now, one methodology is that you ingest the droplets directly, which happened, much during the covid and as well as in pneumonia and other kind of diseases.

04:01 - But there is lot of cases where it actually settles on the surfaces around you. So in order to mimic that, what we did is that we, we actually had this droplets of different types of fluids. So the three different types of fluids that were there in this work is seline, which is basically, salt water, and then of course you have dextrose and new seed. So the rational behind is that seline is your respiratory fluid.

04:27 - So it is mostly of seline new seed is a gastro fluid. So your gastro gastrointestinal system has got mu C and so dextrose in a very similar wave, right? So these are fluids which are commonly, you know, common physiological mediums in which the bacterias basically get nurtured. So you make droplets out of this, okay? I mean, droplets of a particular volume. And then we deploy it on different surfaces. So this could be steamed wood, you know, tomato skin,

05:00 - cucumber skin, anywhere and everywhere, right? And then we allow it to dry under different temperature and relative humidity conditions. So that means the high low temperature, high relative humidity, low relative humidity. Then we use a series of diagnostic techniques, which includes mi microparticle image velocity entry, basically to measure the flow field inside those droplets as these droplets are basically dry, because as, as you dispense these droplets on the surface,

05:28 - they dry over a period of time that is natural. I mean, everything evaporates. So as they dry, they create a flow field inside the droplet, this tiny droplets that you have less than a millimeter size. So these bacterias then get churned inside those droplets, and as they get churn inside those droplets, they form these very spectacular patterns. Some of these things were reported in that paper as well. So they form these spectacular patterns,

05:54 - and depending on the physiological medium that you, it's, or seline or, you know, dextrose, these patterns actually varies. So they, they, they show the spectacular variation in patterns. So what we do is that after everything is dried off, we, we photograph everything. Then we take it for what we call scanning electron microscopy. And we do, you know, atomic force microscopy as well

06:19 - as normal fluoresce imaging, which is confocal imaging. We try to see that where these bacterias are, what planes they are located, and what is a topography of the deposit, and how the deposit basically looks like, because these are very tiny, you cannot see them with your naked eyes. Once all these things are done, then we take these deposits. Now we red dissolve them, and we put it in what we call a cytosis type of a project.

06:46 - firstly study the viability that how many bacterias which were there originally in the droplet, how many of them actually survive after the precipitate forms? So that is a viability count. So you will find that most of the bacterias actually die. I mean, significant percentage actually dies over a period of time. Then we dissolve this, you know, this precipitates, and then we put it in our phagocytosis process,

07:12 - which is a standard immune process that you try to check, to see that how many of these, what is a ulence level of these bacterias? So there we found that the bacterias are very virulent, so whichever ones survive, they become more virulent than the ones that were not in the form. So that was spectacular. So I mean, so it's almost like this, that if you have a hundred bacterias,

07:35 - normally this a hundred bacterias would be viable under normal conditions, but movement, the form of fomite, that means they get dried out of this a hundred, maybe 10 bacterias actually survive, but those 10 have the ence of mold like 30. So that is to give up, I mean, very, you know, global kind of a viewpoint. so then we also do, we also did in vivo experiments, which is basically to feed this precipitates to mouse mice. And we found that the same results actually holds,

08:04 - that means the bacterias becomes more virulent, but many of them actually die in the process. So it's almost like a mini survival of the fittest that is going on, that that means most of the bacterias die, but whichever does not die. They know that, okay, these are the kind of stress conditions we have felt, and therefore we need to be more, more agile, so to say, to survive. So that makes them more, you know, dangerous to mankind.

08:31 - I mean, for the, for the, for animal infections. So that is an interesting question, but that goes more into the physics of the problem. See, that means when this drop, that's actually dry, okay, that precipitate is not a homogenous precipitate anymore because there is something called what we call the coffee strain effect. So that means as the droplet EVAs, there is an outward flow towards the edge of the droplet, which transports most of the bacterias to the edge, right?

08:58 - But some bacterias also remains at the center. So what we found is that, just to give a cut, a long story short, the bacterias, which are at the edge are more, they survive more than the bacterias at the center because they kind of, they're close together. So it must be, there is some sharing of resources that happens and some kind of a stress relieving mechanism that they do, which makes them survive. I mean, the viability part in those bacterias are more than the bacterias at the center.

09:30 - So it is not just one size fits all, even in that small droplet, even in a spatial sense, the central deposit actually has got less viable bacterias compared to the deposits of the edge. So, but obviously, that goes into the nitty of the details. That's why you need to study what it is. And also, another thing we found that, you know, when you have new scene, mu scene is a very sticky substance.

09:55 - This is what, when you cough, this is the, the, the flame that comes out of your mouth. So that is basically new scene. So mucin actually sometimes forms a protective sheet around the bacteria. It's like a c**n kind of a thing. So it protects the bacteria from this, mechanical and osmotic stress and desiccation stress that we call it desiccation stress, is that when you dry something, it gets desiccated,

10:20 - the water actually leaves as a result of that. Like, we can get dehydrated. So that will be like a desiccation process. So the bacteria happens the same way. So this forms a sheep and somehow protects the, you know, the hydration level of the bacteria in a very micro sense. So you always see that when you use mucin compared to seline, bacteria survive more in mu than in seline, because mu seen A is a nutrient rich medium,

10:48 - and b, it perhaps forms this protective sheath around the bacteria protecting it from the harsh environment that we see around. So for the bacteria, it's a harsh environment, so that gives it more longevity, so to say. I mean, so that, that, so the topography therefore becomes very important, not just from a, not just from a system point of view, but also to understand what is exactly going on. So here is a very typical example in which you see fluid

11:16 - mechanics, which is basically your osmotic stress, dessication stress, and your mechanical stress and the flow, they actually alter the bacterial viability and virulence, which is entirely a biological phenomenon. This is basically how the bacteria sees a threat and how it regulates, its metabolic rate, its genes and all those things. But the response function is something that you encounter in everyday life. It is like, it is the same fluid mechanics

11:44 - as we throw a stone or, you know, you know, flow through a pipe, but that influences the bacterial, longevity and the bacterial. So I thought this was a spectacular merging of two fields. If you call it like the, the macroscopic fluid mechanics and the microscopic, biochemistry or microbiology, if you call it, they kind of meet together and they give you the spectacular, spectacular outcome, the bacterias, okay? Always when they are desiccated.

12:14 - And our subsequent works also show the same thing, that if they are desiccated fast, that means if you are in a hostile environment with low relative humidity versus an environment where the relative humidity is kind of a little bit on the higher side, that means it's a slow vaporization process. The bacterias tend to survive more in the higher relative humidity settings. That means when it is nice

12:40 - and easy, that means it's using water, but it has enough time to kind of adjust itself to it. So that is one thing that means, droplet, which is evaporating or a bacteria containing droplet sitting on a surface, which is evaporating in Africa versus in, very humid conditions like, like India, some parts of India, especially in the coastal areas. So they will have different levels of survivability or viability for the exact same bacterial concentration,

13:12 - same bacterial strain, everything. So that is, that is kind of remarkable to begin with. So that matters. So the weather conditions. So one way of saying this is the weather condition matters a lot. Covid has taught us that yes, it matters bacteria, that this, this kind of studies also shows that it matters. The other part is that depending on where the bacteria is residing, that means whether it is a gastro fluid

13:34 - or whether it is coming from your mouth or from other parts of your body that determines its survivability as well, because of the reasons that I mentioned that, you know, forming the sheath and all this, all this, all this stuff. So that chemical composition of the medium also matters as much as the desiccation stress and the fluid mechanics of the problem, as well as the weather conditions. So all this matters.

13:58 - So I would say even a bacteria, for example, in a coastal region, same type of bacteria in a postal region, identical conditions otherwise would actually be more viable and more destructive than the bacteria in some other area. I mean, this is the first, first cut evidence. I mean, this is the point at which it enters the body. After that, of course, our immune system actually takes over. So it depends on the demographics also that some parts

14:24 - of the, you know, some parts of the world, some people are better equipped to handle a disease compared to some other part that is our then our adaptive and innate immunities actually kicking. But from a transmission point of view, the dosage that is entering into your body, that would be higher compared, and that is determined by the weather conditions, chemical stressors, and the mechanical stresses. So after that, What happens is like your, your anatomic

14:53 - and your physiology then takes over, and, that is for the doctors to determine exactly how the proliferation happens after that. But we have seen in our cell lines and individual experiments that that is exactly the case. This should translate into higher, you know, higher disease comes, so to say.

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