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Equality Bill (Money)

Queen’s recommendation signified.

Motion made, and Question put forthwith (Standing Order No. 52(1)(a)),

Question agreed to.

Equality Bill (Carry-over)

Motion made, and Question put forthwith (Standing Order No. 80A(1)(a)),

The Speaker’s opinion as to the decision of the Question being challenged, the Division was deferred until Wednesday 13 May (Standing Order No. 41A).

Business without Debate

Delegated legislation

Ordered,

Ordered,

PETITIONS

General Practice Surgeries (Bedfordshire)

10.28 pm

Andrew Selous (South-West Bedfordshire) (Con): It gives me great pleasure to present a petition signed by more than 3,100 of my constituents from GPs’ surgeries across the South-West Bedfordshire constituency.


11 May 2009 : Column 656

The petition states:

[P000364]

Planning and Development (Plymouth)

10.30 pm

Alison Seabeck (Plymouth, Devonport) (Lab): I rise to bring to the attention of the House concerns that have been generated following the designation by Plymouth city council of a site in Ernesettle as a possible energy-from-waste plant. The petitioners, including members of the action group STIFLE—Stop the Incinerator Fouling Land at Ernesettle—have set out a very detailed case, including planning and environmental concerns, and offered that presentation to the council and the potential contractors for their consideration.

The petition states:

[P000366]


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Penicillin

Motion made, and Question proposed, That this House do now adjourn. —(Steve McCabe.)

10.31 pm

Des Browne (Kilmarnock and Loudoun) (Lab): It is 80 years and one day precisely since Alexander Fleming’s research paper “On the antibacterial action of cultures of a Penicillium” was submitted for publication in The British Journal of Experimental Pathology. In the paper he wrote:

Thus was born the age of antibiotics, although it was to be many years before the first practical application in treatment of bacterial infection in humans, or indeed many years before the coining of the word “antibiotics”. The history tells us much about the nature of scientific discovery, the development of treatments and some of the outside factors that can influence the direction of research, development and human benefit, both positively and negatively.

On 6 August 1881, Alexander Fleming was born at Lochfield farm, near Darvel, the youngest of eight children. He received his first schooling at Loudoun Moor school, went to the village school in Darvel at the age of 10, then two years later, continued his education at Kilmarnock academy. On 24 April this year, standing in the garden of the isolated Lochfield farm, now restored by Phillip and Heather Scott, surveying the landscape that the young Fleming had crossed daily just to get to the place of his early education, I sensed the determination to learn that must have driven him on.

On the same day, examining the contemporary Kilmarnock academy school register, preserved with other Fleming memorabilia by Carole Ford, the head teacher, and Stephen King, the school librarian and archivist, and noting just how many of Fleming’s contemporaries died prematurely of infections, I got a sense of what may have motivated his zeal for fighting those very infections.

Any school that boasts two Nobel laureates merits a special word of public recognition. Kilmarnock academy is entitled to that boast, because of Alexander Fleming and John Boyd Orr, the Scottish teacher, doctor, biologist and politician. When Fleming was 14 he joined an elder brother in London, where after two more years of education he commenced work as a clerk in a shipping company. Four years later, a legacy enabled him to enter St. Mary’s hospital medical school, Paddington, where he excelled in his studies and in numerous sports. He qualified in 1908 and, attracted by research work, entered
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the laboratories of Sir Almroth Wright at St. Mary’s, working on the nature of immunity and the treatment of bacterial infection.

In 1909, the German chemist-physician Paul Ehrlich developed a chemical treatment for syphilis. He had tried hundreds of compounds, and the 666th worked. It was named salvarsan, which means “that which saves by arsenic”. The only previous treatments for the disease had been so toxic as often to kill the patient. Ehrlich brought news of his treatment to London, where Fleming became one of very few physicians to administer salvarsan. He did so with the new and difficult technique of intravenous injection. He soon developed such a busy practice that he got the nickname “Private 606”.

That was the beginning of the age of chemotherapy of infections, with the use of salvarsan, and the beginning of Fleming’s long interest in the use of chemical antiseptics in the treatment of infections, and in ways of aiding the body’s natural protective mechanisms against infection. During the first world war, Fleming served in the Royal Army Medical Corps, working in a laboratory in France to study the treatment of infected war wounds. In 1921, back at St. Mary’s, he discovered lysozyme,

Like Fleming’s discovery of penicillin, his discovery of lysozyme was the result of shrewd observation and the investigation of an unplanned event: he had a cold and observed that the drips from his nose caused lysis of bacteria where they were mixed on the culture plate. He long considered the discovery of lysozyme more important than that of penicillin.

In September 1928, Fleming discovered penicillin when he returned from a six-week holiday and observed the classic clearing or lysis of the bacterial colonies around the contaminating mould, later identified as penicillium notatum. The irony is that modern “good laboratory practice” would probably have dictated that the old culture plates would have been disposed of long since and not left lying around for the mould to grow. The discovery was made and Fleming is reported to have remarked of his observation, “That’s funny.”

Fleming was fortunate as a researcher to have had the freedom to follow up on the unexpected, and his classic 1929 paper includes an extensive study of the production of penicillin by the mould, and of its inhibitory effects against different species of bacteria. However, the crude penicillin was unstable, and Fleming’s laboratory did not have the chemical expertise to purify it in its stable form for further study, so he was unable to pursue its development for clinical use. His later work with penicillin was mainly by using it for selective culture for the isolation of penicillin-insensitive bacteria for study.

Fleming provided samples of the mould to other laboratories, including the Sir William Dunn school of pathology at Oxford. There in 1939, Howard Florey, professor of pathology, and Ernst Chain, a biochemist and refugee from Nazi Germany, began their studies with the purely academic aims of discovering the chemical nature of penicillin and its mode of action. However, they quickly became aware of its clinical potential, and the onset of the second world war brought treatment of infected wounds back into high profile.

With the biochemist Norman Heatley, the Oxford team improvised equipment for bulk culture of the mould, and developed methods for the partial purification
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of penicillin. Fleming was involved in demonstrating the high potency of those penicillin preparations against cultured streptococcus and staphylococcus. By 1941, the Oxford team had purified penicillin to a stable enough form to use on a patient—an Oxford policeman dying of septicaemia. The patient improved markedly, but unfortunately the penicillin ran out, the infection strengthened and the poor man died.

However, by 1943, Fleming was able to use penicillin successfully to treat a girl with streptococcal meningitis; the rapid cure of an almost moribund patient led him to bring penicillin to the notice of the Government. That led to the setting up of the Penicillin Committee and the production of penicillin on an industrial scale, especially in the United States.

Fleming was elected a Fellow of the Royal Society in 1943, knighted in 1944, and shared the 1945 Nobel prize in physiology or medicine with Florey and Chain. In 1945, Fleming was elected the first president of the new Society for General Microbiology, which was formed to provide a common meeting ground for those interested in the study of microbes of all types—bacteria, fungi and viruses and others. The society’s members came from all backgrounds, including medicine, veterinary medicine, agriculture, universities, research institutes and industry.

The society grew rapidly and still thrives today, with more than 5,000 members worldwide. Its main activities are publishing scientific journals, organising conferences, and supporting microbiology education. It is in that context that the society is sponsoring an event for school students in my constituency in November to emphasise the importance of Fleming’s work in the discovery of penicillin, and how that led to an explosion in the discovery of antibiotics, which have brought tremendous benefits in terms of the control of human and animal disease. Over the years, antibiotics must have saved the lives of countless millions of human beings and animals. It is in that context that the society has offered to sponsor prizes for science in both Loudoun academy and Fleming’s old school, Kilmarnock academy.

But what of the future? How secure are we in reliance on antibiotics? The next major step after the introduction of penicillin was the discovery of streptomycin in 1943 by Selman Waksman’s group. He coined the term “antibiotic” for any substance produced by a micro-organism that interferes with the growth of other micro-organisms. Unlike penicillin, which is produced by a fungus, streptomycin was produced by a bacterium. In the 1950s and 1960s, many other antibacterial and anti-fungal agents were discovered in bacteria and fungi in the so-called golden age of antibiotic discovery. In the late 1960s, US Surgeon General William H. Stewart famously stated that we could

and others said similar things. We now know that that is far from being the case for a number of reasons. For a start, he ignored virus diseases, which cannot be treated with antibiotics.

Although thousands of antibiotics have been discovered, and more than 100 are currently approved for medical use, they belong mainly to a rather small number of types of chemical structure, and the rate of discovery in
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the golden age was followed by decades in which far fewer useful natural products were discovered. In the 1990s, drug companies invested heavily in synthetic chemistry and robotic synthesis in attempts to develop “unnatural” new drugs, and in genome sequencing of pathogens to identify genes that encode proteins not present in human cells as possible targets for newly synthesised antibiotics. Those efforts have been disappointing, and have shown little success. It appears that naturally occurring antibiotics and the interactions with their targets have been highly refined in nature over millions of years of natural selection.

More recent methods of trying to create new types of antibiotics include the genetic manipulation of natural products by altering the biosynthetic “assembly line”; the first new products are entering clinical trials. Also, sequencing the genomes of some antibiotic-producing micro-organisms such as streptomyces has shown that there may be “sleeping” antibiotic genes, used only under special conditions infrequently encountered. However, the difficulties of commercial development of any new antibiotics are immense. First, they must be devoid of side effects, unlike new anti-cancer drugs, the drawbacks of which may be considered to be outweighed by benefits. The costs are enormous, and the end product may not be profitable. Many of the antibiotics launched in the 1940s simply would not have been brought to market in the present regulatory climate.

The pressing need for new antibiotics and more types of antibiotics is due to the development of antibiotic resistance in the target pathogens. Methicillin-resistant staphylococcus aureus and multi-drug-resistant human tuberculosis are only two of many examples. Bacteria have evolved over millions of years to survive the insults of their environments, and coping with the production of antibiotics by other micro-organisms has resulted in the evolution of antibiotic resistance mechanisms. Genes for antibiotic resistance have also undoubtedly been transferred between different types of bacteria in the process of horizontal gene transfer.

If we are to maintain and expand our ability to control disease, there is a need for continued research on the fundamental biology of pathogens and their interactions with the host, and on the development of new antibiotics. We could persuade the pharmaceutical industry back to the task by re-examining some of the commercial and regulatory caveats, and develop other mechanisms for disease control such as bacteriophage therapy. The legacy of Fleming and others was the golden age of antibiotic discovery, and all the countless benefits that it brought.

The possibility of a “post-antibiotic age”, brought about by widespread antibiotic resistance in pathogenic bacteria, is scary. In the words of Roy Sleator, writing in the February edition of “Microbiology Today”,

10.45 pm

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