The Antibiotics Crisis: How Did We Get Here And Where Do We Go Next?

In recent years there has been a lot of news about the impending antibiotics crisis, brought to a head by renewed awareness that we are running out of drugs to treat evolving superbugs, and with the startling revelation following the NDM-1 discovery, that microorganisms are also capable of sharing bits of themselves with each other to thwart even our most powerful last-line antibiotics.

Is this the beginning of the end of antibiotics, as some scientists are predicting, are we about to return to a pre-penicillin world where a common bacterial infection could be a death sentence? Or are we just at the cusp of a new wave of inventions that will spur a new generation of drugs that will keep us ahead of the evolutionary race against harmful microorganisms?

This article does not answer these questions, but attempts to present a digest of key facts and recent developments to illuminate the issues around them.

It starts with a summary of what we mean by antibiotics and what they can and cannot treat. It then goes on to explain how antibiotic resistance arises, including the problem of multiple drug resistance, and why many experts say widespread and misguided use is to blame for the accelerated rate at which resistance has become a global problem, as has the dearth in new drug developments. It then describes some of the things researchers and organizations say we can do to to slow down the development of superbugs, and ends with a round up of some surprising new directions that could offer alternative solutions.

Antibiotics and Microorganisms

Antibiotics are drugs that kill microorganisms like bacteria, fungi and parasites. They do

antibiotics

not work against viruses because viruses are not microorganisms. When the press and media talk about antibiotics they generally mean drugs that kill bacteria, because most of the stories that have been hitting the headlines in recent years are about antibiotic-resistant bacteria or “superbugs” like the Methicillin-resistant Staphylococcus aureus (MRSA).

Bacteria on petri dish

Bacteria are very small creatures of usually only one cell, comprising internal cell structures but no distinct nucleus, surrounded by a cell wall. They can make their own proteins and reproduce themselves as long as they have a source of food.

As far as humans are concerned, some bacteria are friendly and essential to wellbeing, they do helpful things like break down food in our gut, while others are dangerous because they attack our tissue and cells to make their food, or they produce toxins that poison and kill.

Some bacteria cause no harm while they live in one part of the body, but then become potentially deadly once they enter the bloodstream. A good example is Escherichia coli (E. coli), which lives in the human gut and helps break down food, but if it enters the bloodstream (eg through a perforation in the intestines), it can cause severe cramping, diarrhea, and even death from peritonitis if not treated promptly.

Another example is Staphylococcus, which lives harmlessly on human skin or even in our nostrils, but if it enters the bloodstream, it can lead to potentially fatal conditions like toxic shock syndrome.

Our immune system has special cells that recognize bacteria as foreign agents and mobilize existing counter-agents or antibodies, or trigger the production of new antibodies, to attack and destroy the bacteria before they get a chance to seize a foothold and start replicating inside us. However, sometimes we lose the fight and succumb to infection, and in some cases, without treatment, the consequences can be very severe and even deadly.

Antibiotics have made a big difference to mankind’s fight against infectious microorganisms and have vastly improved the conditions and chances of success in many fields of medicine all over the world.

They work because they block a life-sustaining function in the unwelcome microorganism. Some stop the microorganism from being able to make or maintain a cell wall, while others target a particular protein that is vital for survival or replication.

An example of the former is penicillin, the first commercially available antibiotic that Alexander Flemming discovered in 1929. Penicillin stops bacteria like Strep (Streptococcus, a bacterium that is commonly found on skin or in the throat) from making strong cell walls. Before the introduction of penicillin in World War II, soldiers were more likely to die of bacterial infections than from their wounds.

Virus

Viruses are not microorganisms, and although capable of self-replicating, do not appear to be “alive” at all: they are particles consisting of DNA or RNA, some long molecules, and a protein coat. They are much smaller than bacteria, have none of their internal cell machinery, and no cell wall. To replicate they have to get inside host cells and hijack their resources.

And here lies a clue as to why we have a global problem with antibiotics and antibiotic resistance: too many doctors and healthcare professionals, often encouraged by patient demand, have been prescribing antibiotics to treat viral infections. This leads to imprudent use of antibiotics and greater opportunity for bacteria to mutate into resistant forms.

Where do we go next?

There is an exciting new approach to the antibiotic crisis that draws no resistance, is a natural mineral and is safe to use.  You can read more about this alternative to antibiotics.

Advertisements

About CareMan
I am the CareMan, have been for 7 years now. I really do care about YOU and getting YOU back to great, natural health, so long as you have an open mind.

Leave a Reply

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

WordPress.com Logo

You are commenting using your WordPress.com 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 )

Google+ photo

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

Connecting to %s

%d bloggers like this: