How did mycobacterium tuberculosis become resistant to antibiotics?

If you’re a fan of medical mysteries, then brace yourself because we’re about to dive into one. Today, we’ll be discussing how the infamous mycobacterium tuberculosis managed to become resistant to antibiotics.

This bacterium has been causing havoc since time immemorial and is responsible for millions of deaths worldwide. It’s basically the Freddy Krueger of infectious diseases – elusive and deadly!

But before I bore you with scientific jargon, let me break it down in simple English: bacteria are organisms that can multiply rapidly in our bodies, making us sick. And antibiotics are drugs used by doctors to kill these bacteria or inhibit their growth.

Pretty straight forward right? So how did this little bugger evolve from being vulnerable to antibiotics into an enemy that laughs in the face of these drugs?

What Is Mycobacterium Tuberculosis?

Mycobacterium tuberculosis is a slow-growing bacterium that mainly affects the lungs but can also attack other parts of the body such as bones and nerves. Its symptoms include persistent coughing (sometimes bloody), fever, night sweats and weight loss. In severe cases, it can result in death.

Now here comes something fascinating: mycobacteria are unique compared with other types because they have a thick protective cell wall made up of lipids (fatty molecules). This feature enables them to survive outside host cells longer than most bacteria – which makes TB highly contagious!

The Rise Of Resistance

As humans evolved over time so have bacteria – constantly adapting themselves due to exposure through mutations or gene transfer between species (which sounds like evolution on steroids!)

Here’s where things get interesting; Antibiotics work by inhibiting essential proteins necessary for bacterial survival and are meant only for killing specific pathogens without harming human tissue. When all goes well; We take antibiotics when there’s an infection and the bacteria die, end of story! (That’s how science works)

However, sometimes a few lucky (or unlucky) bacteria develop random mutations that allow them to survive antibiotics. These survivors divide and pass on their antibiotic-resistant traits to future generations; like parents who give life lessons to their children.

Emergence Of Antibiotic Resistance

“It is not the strongest or smartest species that survive but those most adaptable to change!”
Antibiotic resistance in TB is very complex as it requires several mechanisms such as:
– Drug-inactivating enzymes
– Pump systems that shut out drugs
– Modification/mutation of drug targets
Each time a patient with tuberculosis completes an inadequate course of treatment, this creates favourable conditions for bacterial growth due tocertain strains becoming unresponsive because they had already developed some kind of resistance mechanism (Revered Darwin would be proud!)

But wait there’s more!

Mycobacterium can also exchange genetic information through conjugation plasmids or mobile genetic elements called transposons which have been known to cause trouble – these factors enable extensive acquisition and dissemination between organisms resulting in widespread antibiotic resistance.(On evolution overdrive)

In conclusion our little superbug seems like a bacteriologist’s worst nightmare so always take precautions when interacting with someone coming from areas where there is high prevalence of mycobacteria infections!!!

The Fight Against Tuberculosis Continues

Currently, scientists are working tirelessly researching ways on how we can combat these issues by investing in new technologies such as next generation sequencing (NGS) technology for faster detection & study patterns among others.On top antiretrovirals may reduce both mortality & comorbidity rates.1. As much progress has been made along those lines towards detecting Mycobateriums early There still remains significant barriers including stigma,& poor infrastructures. The fight continues lets keep up the good fight!


1:Yatich NJ, et al. Bull World Health Organ 2019;97:837-847E

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