23. Critically Read the following passage to answer the question (s) Survival of

Question

23. Critically Read the following passage to answer the question (s)

Survival of the Fittest
A typical bacterium reproduces itself every 20 minutes or so, with perhaps one DNA base pair error in every 10 million (107) for each replication. In a typical bacterial population (in a patient) of 100 billion (1011), the number of possible mutations quickly becomes vast. Any one of these might confer a slight advantage for the bacterium (or may lead to its demise), and given the pressure that the pathogenic bacteria came under once the man-made antibiotics were introduced only, as Darwin predicted, would the fittest survive.
Within a few years of their introduction, bacteria developed methods of resistance to each new antibiotic. Some produced enzymes that could destroy or modify the man-made drugs; others developed methods for expulsion of the drugs - eg efflux pumps; while other bacteria developed alternative ways to make cell wall material that circumvented the routes disrupted by the drugs.

The bacteria were given every chance to mutate and improve themselves since they not only met these new drugs in humans, but also in countless millions of farm animals which had been treated with antibiotics to improve their health during intensive growth programmes. Probably one quarter and perhaps as much as one half of all antibiotic use in the last half of the 20th century was in agriculture, and this was exacerbated by prescribing these valuable drugs to people with colds and other viral infections - for which they are useless. In this way the pathogenic bacteria encountered man-made antibiotics on a huge scale and had to mutate or die.

Within three years of the introduction of the penicillins in 1943, the first resistant strains of bacteria had appeared, and most of these employed enzymes - -lactamases - to destroy the essential four-membered lactam ring of the penicillins (see Box 2). It is likely that these enzymes had always existed in certain bacteria as part of the long-standing warfare between bacteria and moulds, but the enzymes now appeared across a wider range of pathogenic bacteria. Very quickly many of the simpler penicillins became useless.

At this point another mould metabolite came to the rescue, ie clavulanic acid (4) from Streptomyces clavuligerus. This natural product had evolved over the millennia to combat the effects of the natural -lactamases since it works as a suicide substrate for this enzyme. In the 1960s Beechams used this natural defence mechanism to counter the effect of the -lactamases through a strategy that used a combination of clavulanic acid and ampicillin (5), which was called Augmentin. The clavulanic acid serves as a suicide substrate for the -lactamases, thus allowing the ampicillin free access to the bacterial cross-linking enzymes (transpeptidases) to inhibit cell wall production. While this is a good example of human ingenuity versus bacterial mutation, it is probably only a matter of time before the pathogenic bacteria mutate to find a way of inactivating clavulanic acid.

The pathogenic bacteria found an even simpler route for modifying aminoglycosides such as streptomycin and gentamycin. Over a period of about 10 years from their introduction, many bacteria underwent genetic changes that led to the production of acetyl transferase or phosphoryl transferase enzymes which acetylated amino groups and phosphorylated hydroxyl groups of the antibiotics as they were administered. The resultant acetylated and phosphorylated drugs were either inactive or much less active than the parent compounds.

What makes the bacteria so effective at overcoming man-made antibiotics is not only the brevity of the replication timescale and their rapid rate of mutation, but also their ability to pass on their resistant genes to other bacteria that they encounter in the mammalian gut and other places. This is why it is so important to finish a course of antibiotics - any bacteria left alive at the end of treatment could survive (in the gut) to pass on their resistant genes to bacteria that do not yet have them. In this way gut bacteria can quickly become multiply resistant to many antibiotics. This is the problem that faces us at the present - most of the really dangerous bacteria have acquired resistance to many if not all of the current armoury of antibiotics. It has taken barely 60 years for these lowly organisms to overcome the chemical ingenuity of mankind with their own ingenious chemistry.
Question A – according to the passage when bacteria were treated with antibiotics which part of the bacteria cell changed the direction of antibiotics when administered in order to survive and thus not be killed off?
Question B – Accoring to the passage, not taking all your antibiotics can lead to resistant bacteria but there are three underlying reasons bacteria can overcome antibiotics. What are those three mechanisms bacteria use to become resistant?

Explanation / Answer

1.The modification of the cell wall is one of the methods by which a bacterium can change the direction of the antibiotic administered. 2. The three ways by which bacteria can gain resistance to antibiotics is: (i) Gain resistance genes from other bacteria (ii) Rapid rate of mutation (iii) Rapid rate of division. The rapid rate of division ensures tht the resistant gene is transferred to all the daughter bacteria. The rapid rate of mutation ensures that the bacteria will somehow try to find some other way to evade the action of antibiotics.

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