Professor sounds warning on infectious diseases
Monday, 4 June 2001
"On only 2 occasions in the history of human life on this planet has the human population actually decreased," says Professor James Paton, from Adelaide University's Department of Molecular Sciences. "On both occasions it was an infectious disease that did it; the Black Death in the 14th Century, and influenza just after the First World War."
Influenza is caused by a virus; the Black Death was a bacterial infection. Infectious diseases caused by bacteria, viruses and parasites continue to kill more people than any other disease group, according to Professor Paton, and globally account for 30% of all deaths.
It is a topic that he will address in his inaugural lecture, "Treatment and prevention of infectious diseases; challenges for the 21st century."
"One shouldn't ignore what is seen as unfashionable areas of research," says Professor James Paton. But how can research into such impressive threats to humanity ever become unfashionable?
"The amount of money going into infectious diseases research is much lower, relative to the number of deaths that they cause, than is the case with more fashionable diseases like cancer," says Professor Paton. "The NHMRC money going into microbiology and immunology research, for example, is probably about 15% of the total."
Infectious diseases can be attacked in different ways. While viruses don't respond to antibiotics, bacteria can. Vaccination protects against both viruses and bacteria, and it is the relative effectiveness of antibiotics and vaccines that interests Professor Paton.
"Infectious diseases are as big a threat to us in western countries as they were fifty years ago," he says." The so-called magic bullet of penicillin is no longer as effective as it was. Bacteria can develop resistance to antibiotics almost as quickly as drug companies with multibillion dollar investment programs can design and test new drugs, so the long term solution is better vaccines."
"With an effective vaccine you only need one dose, rather than having to treat a person with antibiotics every time they get an infection," says Professor Paton. "It is this repeated exposure and large scale administration of antibiotics to the general public which helps to select for resistant organisms," he says.
In fact, the development of antibiotic-resistant bacteria is a graphic demonstration of evolution in action. Bacteria can breed every 20 minutes, and do so in astronomical numbers, but in a population of millions, one or two may mutate or bear a gene resistant to an administered antibiotic. That is all that is required.
While the antibiotic is killing millions of normal organisms, the resistant cell survives and divides. In one hour, it becomes 2, then 4, then 8. In only 24 hours there are once more millions of bacteria, all now carrying the gene that makes them resistant to that antibiotic.
Repeating the treatment with different antibiotics can soon breed a bacterial strain resistant to them all. "We have a situation where infections which were once invariably treatable are now resistant to penicillin and other antibiotics," says Professor Paton. "Tuberculosis is a particular problem because it needs a long course of antibiotic therapy, but patients tend to feel better quite soon and discontinue treatment, so the infection relapses," he says. " That sort of thing selects for antibiotic resistance that builds genetically over the years until you have quite high rates of resistance to a given drug."
Vaccines can have their problems, too. Most use a pathogen which is treated so that it is no longer infective. When it is administered, a patient's immune system forms antibodies against it, and these antibodies recognise and deal with the infective pathogen if it should invade the patient at a later date. It is effective as long as the bacterium doesn't evolve and become unrecognisable, and no other 'unrecognisable' pathogens also invade the patient.
New pneumococcal vaccines used in Africa have been found to protect patients against bacterial types used to prepare the vaccine, "But you get a concomitant increase in disease caused by types which are not included," says Professor Paton, "So you've got to go back to square one and redesign your vaccine," he said. "You have got to understand the biology of the host and pathogen interactions."
Vaccines and antibiotics have been our most trusted weapons in the war against infectious diseases, but others may soon take their place or, at least, assist them.
"We want to look one step further," says Professor Paton. "Are there alternative treatments which we can use, such as blocking interactions between pathogens and hosts?" he asks. "We have been trying to engineer harmless bacteria which can bind toxins produced by pathogenic bacteria in the gut, and prevent those toxins from being absorbed by a patient. It is much more cost effective to put money into an effective vaccine in the long run than to design a drug which will be effective clinically for ten years and then become less useful because of resistance," he maintains.
According to Professor Paton, the more basic research that is carried out on aspects of pathogenesis, the better chance of making sure that the vaccines we use are the most effective, and will not simply delay the problem for another 5 years.
"The issue of a post antibiotic era is a real one," concludes Professor Paton. "Development in antibiotics was the single biggest breakthrough of the 20th Century. As we enter the 21st century there is a real prospect of being without the best outcome of the previous one," he says. "We really are facing the prospect of a large number of diseases having such high rates of resistance that existing drugs will at best only be 50% effective."
Professor Paton took up his position last September as Professor of Microbiology in the department of Molecular Biosciences. His will deliver his inaugural lecture on Friday, 22 June, in Lecture Theatre 102 in the Napier building at 1:15 pm.
Director, Research Centre for Infectious Diseases
School of Molecular & Biomedical Science
The University of Adelaide
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The University of Adelaide
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