By: Sarah McKenna,
on 4/22/2016
The man doing a spot of gardening cleaning out his fishpond in Europe, the woman who becomes unwell after giving birth in rural India, the child with pneumonia in Rwanda, and the senior citizen who develops diverticulitis in Singapore – the triggers are different but they all die from the same disease process: sepsis.
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By: Miranda Dobson,
on 11/19/2015
The serendipitous discovery of Penicillin by Alexander Fleming in 1929 positively transformed modern medicine. Fleming’s decision to spend his summer holiday in East Anglia and his casual approach to laboratory housekeeping was an auspicious combination. After his return to the laboratory he observed that an uncovered culture plate of Staphyloccocus bacteria had been contaminated.
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By: Julia Callaway,
on 11/17/2014
Held every 18 November, European Antibiotics Awareness Day (EAAD) is a European public health initiative that promotes responsible use of antibiotics. The day raises awareness of the threat to public health of antibiotic resistance and encourages prudent antibiotic use.
The number of patients infected by resistant bacteria is growing, which means that antibiotics are losing their effectiveness at an increasing rate. The problem is caused by the inappropriate use and prescribing of antibiotics and is a major threat to patients’ safety and public health. Using antibiotics responsibly can help us to ensure that antibiotics are effective for the use of future generations.
To raise awareness of this vital topic, we’ve put together a reading list of free articles from the Journal of Antimicrobial Chemotherapy, selected by the Editor-in-Chief, Alan Johnson.
Trends in antibiotic prescribing in primary care for clinical syndromes subject to national recommendations to reduce antibiotic resistance, UK 1995–2011: analysis of a large database of primary care consultations by Hawker JI, Smith S, Smith GE et al.
This paper investigates trends in prescribing antibiotics in relation to nationally recommended best practice in the UK. It reports on the mixed success of implementing national guidelines, with prescribing antibiotics for coughs and colds now being greater than before recommendations were made to reduce it.
Good practice recommendations for paediatric outpatient parenteral antibiotic therapy (p-OPAT) in the UK: a consensus statement by Patel S, Abrahamson E, Goldring S et al.
BSAC and the British Paediatric Allergy, Immunity and Infection Group have written recommendations to highlight good clinical practice and governance for managing children on intravenous antimicrobial therapy in secondary or tertiary care settings. Managing children on intravenous antimicrobial therapy at home can improve parent and patient satisfaction and reduce health-care associated infections.
Longitudinal trends and cross-sectional analysis of English national hospital antibacterial use over 5 years (2008–13): working towards hospital prescribing quality measures by Cooke J, Stephens P, Ashiru-Oredope D. et al.
This study examines the variation in antimicrobial use in individual hospitals in the UK. It uncovers a wide variation in usage between individual hospitals and recommends the urgent development of quality measures of optimal hospital antimicrobial prescribing.
Evaluation of antifungal use in a tertiary care institution: antifungal stewardship urgently needed by Valerio M, Rodriguez-Gonzalez CG, Muñoz P et al.
This article explores the quality of antifungal use and reports on antifungals being prescribed unnecessarily in 16% of cases. It considers the potential savings that could be made by optimising antifungal therapy.
Effect of antibiotic stewardship programmes on Clostridium difficile incidence: a systematic review and meta-analysis by Feazel LM, Malhotra A, Perencevich EN et al.
Despite vigorous infection control measures, Clostridium difficile continues to cause significant disease burden. This paper demonstrates that restrictive antibiotic stewardship programmes can be used to reduce the risk of Clostridium difficile infections.
A window into the lives of junior doctors: narrative interviews exploring antimicrobial prescribing experiences by Mattick K, Kelly N, Rees C et al.
Prescribing medications is an important challenge in the transition to junior doctor practice. This study explores the antimicrobial prescribing experiences of foundation year doctors in two UK hospitals and offers some practical solutions to the challenges they face.
Impact of implementation of a novel antimicrobial stewardship tool on antibiotic use in nursing homes: a prospective cluster randomized control pilot study by Fleet E, Rao GG, Patel B et al.
This paper evaluates the impact of ‘Resident Antimicrobial Management Plan’, a novel antimicrobial stewardship tool on systemic antibiotic use for treatment of infection in nursing homes. This pilot study demonstrated that the use of this tool was associated with a significant increase in total antibiotic consumption.
Antibiotic use in Dutch primary care: relation between diagnosis, consultation and treatment by van den Broek d’Obrenan J, Verheij TJ, Numans ME et al.
The aim of this study was to describe the antibiotic management of infectious diseases in the clinical context in the Netherlands. It examines trends in prescribing antibiotics for different types of infection and concludes that complete data on infectious disease management, with respect to patient and physician behaviour, are crucial for understanding changes in antibiotic use, and in defining strategies to reduce inappropriate antibiotic use.
Effect of antibiotic streamlining on patient outcome in pneumococcal bacteraemia by Cremers AJH, Sprong T, Schouten JA et al.
This study investigated whether streamlining in bacteraemic pneumococcal infections is associated with mortality. This practice can reduce the use of broad-spectrum antibiotics but is poorly undertaken due to lack of clarity related to patient safety.
The efficacy of non-carbapenem antibiotics for the treatment of community-onset acute pyelonephritis due to extended-spectrum β-lactamase-producing by Park SH, Choi SM, Chang YK et al.
Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli has become an important cause of community-onset urinary tract infections. This study aimed to evaluate the effectiveness of non-carbapenem antibiotics for acute pyelonephritis (APN) due to ESBL-producing E. coli.
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By: DanP,
on 8/7/2014
Despite the huge body of evidence that males and females have very different immune systems and responses, few biomedical studies consider sex in their analyses. Sex refers to the intrinsic characteristics that distinguish males from females, whereas gender refers to the socially determined behaviour, roles, or activities that males and females adopt. Male and female immune systems are not the same leading to clear sexual dimorphism in response to infections and vaccination.
In 2010, Nature featured a series of articles aimed at raising awareness of the inherent sex bias in modern day biomedical research and, yet, little has changed since that time. They suggested journals and funders should insist on studies being conducted in both sexes, or that authors should state the sex of animals used in their studies, but, unfortunately, this was not widely adopted.
Even before birth, intrauterine differences begin to differentially shape male and female immune systems. The male intrauterine environment is more inflammatory than that of females, male fetuses produce more androgens and have higher IgE levels, all of which lead to sexual dimorphism before birth. Furthermore, male fetuses have been shown to undergo more epigenetic changes than females with decreased methylation of many immune response genes, probably due to physiological differences.
The X chromosome contains numerous immune response genes, while the Y chromosome encodes for a number of inflammatory pathway genes that can only be expressed in males. Females have two X chromosomes, one of which is inactivated, usually leading to expression of the wild type gene. X inactivation is incomplete or variable, which is thought to contribute to greater inflammatory responses among females. The immunological X and Y chromosome effects will begin to manifest in the womb leading to the sex differences in immunity from birth, which continue throughout life.
MicroRNAs (miRNAs) regulate physiological processes, including cell growth, differentiation, metabolism and apoptosis. Males and females differ in their miRNA expression, even in embryonic stem cells, which is likely to contribute to sex differences in the prevalence, pathogenesis and outcome of infections and vaccination.
Females are born with higher oestriol concentrations than males, while males have more testosterone. Shortly after birth, male infants undergo a ‘mini-puberty’, characterised by a testosterone surge, which peaks at about 3 months of age, while the female effect is variable. Once puberty begins, the ovarian hormones such as oestrogen dominate in females, while testicular-derived androgens dominate in males. Many immune cells express sex hormone receptors, allowing the sex hormones to influence immunity. Very broadly, oestrogens are Th2 biasing and pro-inflammatory, whereas testosterone is Th1 skewing and immunosuppressive. Thus, sex steroids undoubtedly play a major role in sexual dimorphism in immunity throughout life.
Sex differences have been described for almost every commercially available vaccine in use. Females have higher antibody responses to certain vaccines, such as measles, hepatitis B, influenza and tetanus vaccines, while males have better antibody responses to yellow fever, pneumococcal polysaccharide, and meningococcal A and C vaccines. However, the data are conflicting with some studies showing sex effects, whereas other studies show none. Post-vaccination clinical attack rates also vary by sex with females suffering less influenza and males experiencing less pneumococcal disease after vaccination. Females suffer more adverse events to certain vaccines, such as oral polio vaccine and influenza vaccine, while males have more adverse events to other vaccines, such as yellow fever vaccine, suggesting the sex effect varies according to the vaccine given. The existing data hint at higher vaccine-related adverse events in infant males progressing to a female preponderance from adolescence, suggesting a hormonal effect, but this has not been confirmed.
If male and female immune systems behave in opposing directions then clearly analysing them together may well cause effects and responses to be cancelled out. Separate analysis by sex would detect effects that were not seen in the combined analysis. Furthermore, a dominant effect in one of the sexes might be wrongly attributed to both sexes. For drug and vaccine trials this could have serious implications.
Given the huge body of evidence that males and females are so different, why do most scientific studies fail to analyse by sex? Traditionally in science the sexes have been regarded as being equal and the main concern has been to recruit the same number of males and females into studies. Adult females are often not enrolled into drug and vaccine trials because of the potential interference of hormones of the menstrual cycle or risk of pregnancy; thus, most data come from trials conducted in males only. Similarly, the majority of animal studies are conducted in males, although many animal studies fail to disclose the sex of the animals used. Analysing data by sex adds the major disadvantage that sample sizes would need to double in order to have sufficient power to detect significant sex effects. This potentially means double the cost and double the time to conduct the study, in a time when research funding is limited and hard to obtain. Furthermore, since the funders don’t request analysis by sex, and the journals do not ask for it, it is not a major priority in today’s highly competitive research environment.
It is likely that we are missing important scientific information by not investigating more comprehensively how males and females differ in immunological and clinical trials. We are entering an era in which there is increasing discussion regarding personalised medicine. Therefore, it is quite reasonable to imagine that females and males might benefit differently from certain interventions such as vaccines, immunotherapies and drugs. The mindset of the scientific community needs to shift. I appeal to readers to take heed and start to turn the tide in the direction whereby analysis by sex becomes the norm for all immunological and clinical studies. The knowledge gained would be of huge scientific and clinical importance.
Dr Katie Flanagan leads the Infectious Diseases Service at Launceston General Hospital in Tasmania, and is an Adjunct Senior Lecturer in the Department of Immunology at Monash University in Melbourne. She obtained a degree in Physiological Sciences from Oxford University in 1988, and her MBBS from the University of London in 1992. She is a UK and Australia accredited Infectious Diseases Physician. She did a PhD in malaria immunology based at Oxford University (1997 – 2000). She was previously Head of Infant Immunology Research at the MRC Laboratories in The Gambia from 2005-11 where she conducted multiple vaccine trials in neonates and infants.
Dr Katie Flanagan’s editorial, ‘Sexual dimorphism in biomedical research: a call to analyse by sex’, is published in the July issue of Transactions of the Royal Society of Tropical Medicine and Hygiene. Transactions of the Royal Society of Tropical Medicine and Hygiene publishes authoritative and impactful original, peer-reviewed articles and reviews on all aspects of tropical medicine.
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By: Hannah Paget,
on 7/25/2014
We humans have a love-hate relationship with bugs. I’m not talking about insects — although many of us cringe at the thought of them too — but rather the bugs we can’t see, the ones that make us sick.
Sure, microorganisms give us beer, wine, cheese, and yoghurt; hardly a day goes by without most people consuming food or drink produced by microbial fermentation. And we put microbes to good use in the laboratory, as vehicles for the production of insulin and other life-saving drugs, for example.
But microbes are also responsible for much of what ails us, from annoying stomach ‘bugs’ to deadly infectious diseases such as tuberculosis and plague. Bacteria and viruses are even linked to certain cancers. Bugs are bad; antibiotics and antivirals are good. We spend billions annually trying to rid ourselves of microorganisms, and if they were to all disappear, well, all the better, right?
This is, of course, nonsense. Even the most ardent germaphobe would take a deep breath and accept the fact that we could no more survive without microbes than we could without oxygen. No matter how clean we strive to be, there are 100 trillion bacterial cells living on and within our bodies, 10 times the number of human cells that comprise ‘us’. Hundreds of different bacterial species live within our intestines, hundreds more thrive in our mouths and on our skin. Add in the resident viruses, fungi, and small animals such as worms and mites, and the human body becomes a full-blown ecosystem, a microcosm of the world around us. And like any ecosystem, if thrown off-balance bad things can happen. For example, many of our ‘good’ bacteria help us metabolize food and fight off illness. But after a prolonged course of antibiotics such bacteria can be knocked flat, and normally benign species such as ‘Clostridium difficile’ can grow out of control and cause disease.
Given the complexity of our body jungle, some researchers go as far as to propose that there is no such thing as a ‘human being’. Each of us should instead be thought of as a human-microbe symbiosis, a complex biological relationship in which neither partner can survive without the other. As disturbing a notion as this may be, one thing is indisputable: we depend on our microbiome and it depends on us.
And there is an even more fundamental way in which the survival of Homo sapiens is intimately tied to the hidden microbial majority of life. Each and every one of our 10 trillion cells betrays its microbial ancestry in harboring mitochondria, tiny subcellular factories that use oxygen to convert our food into ATP, the energy currency of all living cells. Our mitochondria are, in essence, domesticated bacteria — oxygen-consuming bacteria that took up residence inside another bacterium more than a billion years ago and never left. We know this because mitochondria possess tiny remnants of bacterium-like DNA inside them, distinct from the DNA housed in the cell nucleus. Modern genetic investigations have revealed that mitochondria are a throwback to a time before complex animals, plants, or fungi had arisen, a time when life was exclusively microbial.
As we ponder the bacterial nature of our mitochondria, it is also instructive to consider where the oxygen they so depend on actually comes from. The answer is photosynthesis. Within the cells of plants and algae are the all-important chloroplasts, green-tinged, DNA-containing factories that absorb sunlight, fix carbon dioxide, and pump oxygen into the atmosphere by the truckload. Most of the oxygen we breathe comes from the photosynthetic activities of these plants and algae—and like mitochondria, chloroplasts are derived from bacteria by symbiosis. The genetic signature written within chloroplast DNA links them to the myriad of free-living cyanobacteria drifting in the world’s oceans. Photosynthesis and respiration are the biochemical yin and yang of life on Earth. The energy that flows through chloroplasts and mitochondria connects life in the furthest corners of the biosphere.
For all our biological sophistication and intelligence, one could argue that we humans are little more than the sum of the individual cells from which we are built. And as is the case for all other complex multicellular organisms, our existence is inexorably linked to the sea of microbes that share our physical space. It is a reality we come by honestly. As we struggle to tame and exploit the microbial world, we would do well to remember that symbiosis—the living together of distinct organisms—explains both what we are and how we got here.
John Archibald is Professor of Biochemistry and Molecular Biology at Dalhousie University and a Senior Fellow of the Canadian Institute for Advanced Research, Program in Integrated Microbial Biodiversity. He is an Associate Editor for Genome Biology & Evolution and an Editorial Board Member of various scientific journals, including Current Biology, Eukaryotic Cell, and BMC Biology. He is the author of One Plus One Equals One: Symbiosis and the Evolution of Complex Life.
Image credit: Virus Microbiology. Public domain via Pixabay
The post Microbes matter appeared first on OUPblog.
By: Alice,
on 3/28/2014
It is almost impossible to read a daily newspaper or listen to news reports from television and radio without hearing about an outbreak of an infectious disease. On 13 March 2014, the New York City Department of Health investigated a measles outbreak. Sixteen cases including nine pediatric cases were detected, probably caused by a failure to vaccinate the victims. On 12 February, an outbreak of a common microbial pathogen known as C.difficile occurred in several hospitals in Great Britain. This pathogen induces severe cases of gastrointestinal distress including diarrhea, fever, and stomach cramps. One of the main problems with a number of microbial pathogens like C.difficile is that they have become completely resistant to many known drugs.
How did this occur? Antibiotics, complex substances produced by certain types of microbes that destroy other microbes, were hailed as miracle drugs when the first one (penicillin) was discovered more than 70 years ago by Alexander Flemming. Although over 70 useful antibiotics have been discovered since penicillin, many can no longer be used because microbial pathogens have become resistant to them through evolution. In fact, over two million people in the United States become infected with antibiotic resistant pathogens every year, leading to 23,000 deaths according to the Centers for Disease Control and Prevention (CDC). New non-antibiotic drugs are always being sought to treat infectious diseases (mostly microbial because viral diseases are not susceptible to antibiotics). One such new discovery is a commonly used pain medication called Carprofen which inhibits antibiotic resistant pathogens. Thus, the “war against” infectious diseases remains an ongoing focus of medical research.
Of course there are many other pathogens (both microbial and viral) besides those mentioned above that assault us and our body defenses constantly. They include pneumonia, dysentery, tuberculosis, tetanus, diphtheria, scarlet fever, ulcers, typhoid, meningitis, plague, cholera (bacterial), polio, HIV (AIDS), rabies, influenza, measles, mumps, the common cold, yellow fever, and chicken pox (viral). Nevertheless, all of us are not equally “susceptible” to each infectious disease — a poorly understood term that determines why some of us get one disease but not another, or why some diseases occur in the winter while others occur in the summer.
This brings us to an important concept, namely, that there is no way to be free of microbes that inhabit every “nook and cranny” of our bodies. Of the approximately ten million cells that make up the human body, there are billions of microbes that come along with them. Most microbes that inhabit our bodies are necessary for our existence. Together they make up what is called the “microbiome” consisting of a diverse group of microbes that help keep each of us healthy. Most of them are found in the gastrointestinal tract where they aid digestion; synthesize vitamins and other necessary biochemicals our cells cannot make; attack and destroy pathogens; and stimulate our immune system to act in the same way.
Nevertheless, with this constant assault, one might wonder how it is possible we have survived for so long. There are a number of other variables besides the “microbiome’ that are responsible and that are still poorly understood. These include an ability of a host (us) to coexist with a pathogen (we keep them at bay or limit their spread internally like tuberculosis), an ability to mount a furious immunological attack on the pathogen to destroy them, or an innate ability to remain “healthy” (a vague term that really signifies the fact that all of our metabolic systems are operating optimally most of the time like digestion, excretion, blood circulation, neurological or brain function, and healthy gums and teeth among other systems).
Where does this innate ability come from? Simply put, genetic phenomena (both in microbes and in humans). These traits are not only inherited under the control of genes but their functions are also controlled by such genes. Different pathogens have different sets of genes which act to produce a specific disease in a susceptible host. However, it is also why individual hosts (humans) are more or less resistant to such infectious diseases.
How does the body interact with these “foreign” entities? The immune system must protect the body from attack by pathogens and also from the formation of abnormal cells which could turn cancerous. Two types of immune responses exist. One is under the control of antibodies (proteins which circulate in the blood stream) that resist and inactivate invading pathogens by binding to them. The other is mediated by a certain type of white blood cell called a lymphocyte that destroys abnormal (potentially cancerous) cells and viral infected cells. Together, with other white blood cells, they present a formidable defense against infection and abnormality.
It takes time for an immune response by antibodies to develop during a pathogenic invasion because there are many components involved in the activity. They are usually divided into primary and secondary responses. The primary response represents the first contact with the antigen which after a period of time results in an increased production of specific antibodies that react only to that antigen (which by the way are also produced by certain lymphocytes called “B” or plasma cells). Once the infection is controlled, antibody levels fall considerably. If, however, another infection occurs in the future by the same pathogen, a much more vigorous response will result (called the secondary response) producing a much faster development and a higher level of antibodies. Why is the secondary response so much faster and vigorous? This phenomenon is due to a remarkable property of the immune system in which the primary response is “remembered” after its decrease by the preservation of “memory” “B” lymphocytes that circulate until the secondary response occurs, no matter how long it takes.
William Firshein is the Daniel Ayers Professor of Biology, Emeritus and author of The Infectious Microbe. He chaired the Biology Department at Wesleyan University for six years and published over 75 original research papers in the field of Molecular Microbiology of Pathogens. He was the recipient of several million dollars of grant support from various public and private research agencies and taught over 6,000 graduate and undergraduate students during his 48 year career.
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By: ChloeF,
on 11/30/2012
What do anaesthetists do? How does anaesthesia work? What are the risks? Anaesthesia is a mysterious and sometimes threatening process. We spoke to anaesthetist and author Aidan O’Donnell, who addresses some of the common myths and thoughts surrounding anaesthesia.
On the science of anaesthesia:
Click here to view the embedded video.
The pros and cons of pain relief in childbirth:
Click here to view the embedded video.
Are anaesthetists heroes?
Click here to view the embedded video.
Aidan O’Donnell is a consultant anaesthetist and medical writer with a special interest in anaesthesia for childbirth. He graduated from Edinburgh in 1996 and trained in Scotland and New Zealand. He now lives and works in New Zealand. He was admitted as a Fellow of the Royal College of Anaesthetists in 2002 and a Fellow of the Australian and New Zealand College of Anaesthetists in 2011. Anaesthesia: A Very Short Introduction is his first book. You can also read his blog post Propofol and the Death of Michael Jackson.
The Very Short Introductions (VSI) series combines a small format with authoritative analysis and big ideas for hundreds of topic areas. Written by our expert authors, these books can change the way you think about the things that interest you and are the perfect introduction to subjects you previously knew nothing about. Grow your knowledge with OUPblog and the VSI series every Friday!
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By: Alice,
on 2/12/2012
Italian panel depicting Charles Darwin, created ca. 1890, on display at the Turin Museum of Human Anatomy. Source: Wikimedia Commons.
Today is Darwin’s birthday. It’s doubtful that any scientist would deny Darwin’s importance, that his work provides the field of biology with its core structure, by providing a beautiful, powerful mechanism to explain the diversity of form and function that we see all around us in the living world. But being of importance to one’s field is only one way we judge a scientist’s contributions. There is also the matter of how their work has changed lives all over the world, even of those who don’t know or necessarily care about their accomplishments. What has Darwin done for his fellow human beings? Why should they care about what he showed us, or want to learn what he had to teach?
Understanding evolution is challenging, for many reasons. We often point to the religious questions raised by his work as the cause of these difficulties, but there are many more. No creature decides to change their DNA, nor can a species foresee what they should become to survive, but it sure seems like they do. Evolution provides such elegant solutions to incredibly complex problems, it’s hard to see them as the product of random variation and selection. Even for people who lack religious convictions that make evolution discomforting, it’s hard to grasp the mechanisms of evolution. This difficulty arises out of developmental constraints that lead us to look for centralized, intentional agents when we make causal attributions. It comes out of the challenges inherent in altering our conceptions of the world and replacing one belief system with another, and out of the emotional reaction we have to facing the reality that we are not special or superior to our biological cousins, nor are we in control of the fate of our species in generations to come.
If we’re going to ask people to expend the time and effort it requires to wrap their heads around a idea like biological evolution, it seems as though there ought to be a really big payoff for all that work. So, what does learning about evolution get us?
We’ve asked this question to quite a few teachers, biologists, philosophers, and educational researchers along the course of several projects, the most extensive and recent being the one that led to the edited volume OUP will be putting out soon on teaching and learning about evolution. The reaction is almost always the same. First, there is the pause, as they blink, startled that anyone would be asking such a thing. Often they call upon evolution’s importance to science, and its beauty and elegance — who wouldn’t want to spend their time contemplating that? But if pushed back, and asked what practical value they could point to that would make the struggle of mastering these complex ideas worthwhile, they have a hard time coming up with an answer. The most common responses revolve around the (mis)use of antibiotics, and that people need to know that taking these drugs too often could cause real long-term harm. The second most popular argument is that people should understand the importance of biodiversity, how fragile species become when their gene pool dwindles and ecological balances are disrupted, and that being a part of nature — not above it — comes with responsibili
By: Kirsty,
on 5/6/2009
John Playfair’s short book Living with Germs: In Health and Disease takes the reader through the essentials of infectious organisms - bacteria, viruses, protozoa and the rest - and of our defences against them, the immune system with its powerful weapons and occasionally dangerous side effects. The alternatives - antibiotics and public health measures - are also considered and there is a look ahead at some of the significant problems to come in the future. In the post below, John Playfair reminds us that infectious diseases don’t stand still for long.
The death of two sumo wrestlers last year from a new strain of herpes gladiatorum (’scrumpox’ to rugby players) is not only bad news for Japan’s number one sport but a reminder that infectious diseases do not stand still for long.
MRSA, drug-resistant tuberculosis, malaria, and the permanently shifting AIDS viruses have been for years at the very top of the list of world health problems, and now a new hybrid flu virus from pigs, containing additional genes from both avian and human strains has unexpectedly leapfrogged all these to potential pandemic status (WHO threat level 5). With global warming already introducing ‘tropical’ insect-borne diseases such as malaria, leishmaniasis, and dengue to temperate zones such as Europe and North America, and with vaccines still lacking for all fungal, protozoal, and worm infections, it is no longer thinkable to say, as the US Surgeon-General rashly did 40 years ago, that ‘it is time to close the book on infectious diseases.’
Three problems stand out. Drugs - loosely known as ‘antibiotics’ - have been very successful against some bacterial infections but much less so against viruses, where years of expensive research have been needed to identify those few weak spots where a drug can damage the virus but not its host (bacteria have far more of these). Vaccines, on the contrary, have a better record against viruses than against bacteria, and if any more infections are to follow smallpox into oblivion they will probably be viral - polio and the common childhood viruses being the most likely candidates. There remains the stumbling block of the immune system, our main protection against infection and the point at which successful vaccines operate. Almost a century ago it was discovered that with ‘toxic’ diseases like diphtheria and tetanus, all you needed for protection was a sufficient level of antibody in the blood.
But unfortunately this is not true of many infections: antibody may be ineffective, or directed at the wrong target, or actually harmful. Sometimes immune cells must go into action, killing viruses or releasing messenger molecules known as cytokines. But even cytokines can be dangerous; in fact they may account for the curious fact that swine flu appears to be more deadly in younger victims with active immune systems. So we must be prepared for more surprises.
