Stuff that isn’t from openevidence

Disease Stuff - Brought to you by totalnoobSorry a lot of this isn’t highlighted

General No ImpactDiseases won’t cause extinction – burnout or variationYork, 6/4/2014 (Ian, head of the Influenza Molecular Virology and Vaccines team in the Immunology and Pathogenesis Branch, Influenza Division at the CDC, former assistant professor in immunology/virology/molecular biology (MSU), former RA Professor in antiviral and antitumor immunity (UMass Medical School), Research Fellow (Harvard), Ph.D., Virology (McMaster), M.Sc., Immunology (Guelph), “Why Don't Diseases Completely Wipe Out Species?” 6/4, http://www.quora.com/Why-dont-diseases-completely-wipe-out-species#THUR)

But mostly diseases don't drive species extinct . There are several reasons for that. For one, the most dangerous diseases are those that spread from one individual to another. If the disease is highly lethal, then the population

drops, and it becomes less likely that individuals will contact each other during the infectious phase. Highly contagious diseases tend to burn themselves out that way. Probably the main reason is variation . Within the host and the pathogen population there will be a wide range of variants. Some hosts may be naturally

resistant. Some pathogens will be less virulent. And either alone or in combination, you end up with infected individuals who survive . We see this in HIV , for example. There is a small fraction of humans who

are naturally resistant or altogether immune to HIV, either because of their CCR5 allele or their MHC Class I type. And there are a handful of people who were infected with defective versions of HIV that didn't progress to disease . We can see

indications of this sort of thing happening in the past, because our genomes contain many instances of pathogen resistance genes that have spread through the whole population . Those all started off as rare mutations that conferred a strong selection advantage to the carriers, meaning that the specific infectious diseases were serious threats to the species.

And, international actors checkWayne, 2014 (Alex, syndicated columnist on US health policy, “Global Effort Signed to Halt Spread of Infectious Disease,” Bloomber, 2/13, http://www.bloomberg.com/news/2014-02-13/global-effort-signed-to-halt-spread-of-infectious-disease.html#THUR)

The U.S. won commitments from 25 countries and the W orld Health Organization to work together on systems to better detect and combat outbreaks of infectious disease s such as H7N9 avian flu and Ebola virus. The Obama

administration plans to spend $40 million in 10 countries this year to upgrade laboratories and communications networks so outbreaks can be controlled more quickly , Thomas Frieden, director of the Centers for Disease Control and Prevention, said today in

an interview. President Barack Obama will seek another $45 million next year to expand the program. Infectious diseases account for about 1 in 4 deaths worldwide, according to the U.S. National Institutes of Health. While diseases such as Ebola and Severe Acute Respiratory Syndrome haven’t posed a threat to the U.S., lapses in other

countries may allow an outbreak to spread rapidly, Frieden said. “No country can protect itself solely within its borders,” Frieden said. “We’re all only as safe as the weakest link out there. This is an effort to essentially make the U.S. safer and make the world safer, to improve countries’ capacity to better find, stop and prevent health threats .” Frieden and Kathleen Sebelius, the U.S. health

secretary, held a videoconference today with the partners in the effort. While no other country made a specific financial commitment today, Frieden said, all the nations at the conference including China, Russia, France and the U.K. agreed to “ accelerate progress and address not just the health sector but include security in health in new ways .” First Consensus “For the first time, really, we have a consensus on not only what are the threats, but what do we have to do to address them, ” he said. As an example, Frieden said Turkey’s government agreed to host a WHO office to respond to outbreaks in its region. The agreement will also target emerging infections such as Middle East Respiratory Syndrome. The 10 countries in line for the U.S. investment, which

will be funded by the CDC and the Department of Defense, weren’t identified. The CDC plans to build on test projects last year in Uganda and Vietnam,

where the agency helped the two nations’ health officials improve systems to detect and combat outbreaks of dangerous pathogens that include drug-resistant tuberculosis, Ebola virus and exotic flu strains. In Uganda, CDC officials helped the country’s Ministry of Health upgrade laboratories where tissue samples would be tested in the event of an outbreak, and developed a system for local doctors to report cases of illness by text message, according to an article published in the CDC’s journal Morbidity and Mortality

Weekly Report. Uganda now is able to quickly transport tissue samples from rural outbreaks to a high-security lab in the capital, Kampala, by motorcycle courier and overnight mail, Frieden said. A mobile phone network-connected printer then texts lab results back to rural hospitals, he said.

“Ultimately every country in the world should have this kind of system,” Frieden said. The $ 40 million ,

he said, “ is certainly enough to make a good start.”

SARS changed everything – created effective mechanisms and political will for multilateral cooperation to survey, contain and treat diseaseRoos, 2013 (Robert, medical editor, master's degree in science journalism (Minnesota), fellow at the Center for Infectious Disease Research and Policy, “Experts: SARS Sparked Global Cooperation to Fight Disease,” Minnesota Center for Infectious Disease Research and Policy, 4/15, http://www.cidrap.umn.edu/news-perspective/2013/04/experts-sars-sparked-global-cooperation-fight-disease#THUR)

A new set of journal articles related to the 10th anniversary of the SARS epidemic in 2003 says the episode did much to boost recognition of the need for coordinated international and national responses to emerging infectious diseases. The articles and commentaries in Emerging Infectious Diseases reflect on the effects of SARS (severe acute respiratory syndrome), which arose in China in late 2002 and spread to more than 30 countries in early 2003, sickening about 8,000 people and killing around 800. The outbreak was first publicized by the World Health Organization (WHO) on Mar 12, 2003. Among the reports is one describing two new SARS-like coronaviruses—close relatives of the SARS coronavirus—found in bats in China. The new viruses are more distant relatives of the novel human coronavirus that has caused illnesses in 17 people, with 11 deaths, in the past year. All of

the cases had connections to the Middle East. Publication of the articles comes as the world is contending with still another emerging pathogen, the novel H7N9 influenza virus in China, which has infected at least 64 people and killed 14 in recent weeks. Surveillance

and response In a "synopsis" piece, a team led by Christopher R. Braden, MD, of the US Centers for Disease Control and Prevention (CDC) reports on progress in global surveillance and response capacity in the 10 years since SARS emerged. They review the milestones of the epidemic, from its silent emergence in southern China in November 2002 to its spread to Hong Kong and, boosted by a "superspreader," from there

to many other countries. They say the SARS epidemic powerfully stimulated international cooperation to fight emerging diseases . "Perhaps the most important legacy of SARS is the recognition of the critical need for a multilateral response, led by WHO, in the event of a rapidly moving but ultimately containable global epidemic," they write. "The central role of WHO in coordinating the laboratory network that identified the etiologic agent and shared reagents, the epidemiology network that characterized the spread and identified the most effective control measures, and the policy and communications network that

incorporated rapidly changing knowledge into measured travel advisories was critical for the control of the epidemic and a credit to WHO. " The SARS epidemic dramatically reduced global travel and business, showing how disruptive a new pathogen could be, Braden and colleagues

observe. Those effects stimulated pandemic flu planning and surveillance, a greater focus on global health security, and improved laboratory and surveillance networks. Further , the episode spurred efforts to update the International Health Regulations, which had not been revised since 1969 , the article says. The regulations took effect in 2007. However, fewer than 20% of the 194 WHO countries that accepted the regulations had complied with their core requirements by

the June 2012 deadline, according to Braden and colleagues. Another effect of SARS was to spur the establishment of new national public health agencies in Canada (the Public Health Agency of Canada, or PHAC) and the United Kingdom (the Health

Protection Agency), the authors say. In a related perspective article, a team led by Jeffrey P. Koplan, MD, MPH, of Emory University, a former CDC director,

says the value of national public health institutes was one of the major lessons of SARS. Koplan is joined by authors

from the PHAC and its counterparts in Hong Kong and China. They note that more than 80 national public health institutes are now linked through the International Association of National Public Health Institutes, which promotes the establishment of new institutes and helps strengthen existing ones.

No Pandemic Extinction --- Our evidence assumes mutations and unlikely worst case scenariosBrooks 12 (Michael Brooks, Consultant for New Scientist, “Deep future: Why we'll still be here,” New Scientist, Volume 213, Issue 2854, March, p. 36–37, Science Direct)//NR

We are also unlikely to be extinguished by a killer virus pandemic . The worst pandemics occur when a new strain of flu virus spreads across the globe. In this scenario people have no immunity , leaving

large populations exposed. Four such events have occurred in the last 100 years – the worst, the 1918

flu pandemic, kil led less than 6 per cent of the world's population . More will come, but disease-led extinctions of an entire species only occur when the population is confined to a small area, such as an

island. A severe outbreak will kill many millions but there is no compelling reason to think any future

virus mutations will trigger our total demise .

Disease can’t cause extinction – epidemiology provesLenihan et al 13 (Professor of Applied UC Santa Barbra, Tal Ben-Horin, Post Doctoral Researcher, Kevin Lafferty Research ecologist USGS, “Variable intertidal temperature explains why disease endangers¶ black abalone” in Ecology, http://hsrl.rutgers.edu/abstracts.articles/Ben-Horin.et.al.2013.ecology.pdf \\ME)

Epidemiological theory holds that host-specific infectious ¶ diseases will rarely drive hosts to extinction ¶ because transmission eventually breaks down due to a ¶ decline in susceptible hosts (Anderson and May 1992, de¶ Castro and

Bolker 2005). This phenomenon, known as¶ epizootic fade out, implies that a disease will die out ¶ when the host population falls below a threshold density ¶ (Lloyd-Smith et al. 2005). Accordingly, infectious ¶ diseases have played only a minor role in global species ¶ loss , and have rarely provided the sole cause of threat ¶ for species listed under either the U.S. Endangered¶ Species Act or IUCN

Red List of Threatened Species¶ (Smith et al. 2006). Yet there are cases of infectious¶ diseases threatening species with extinction on local¶ scales (McCallum et al. 2009). In these cases, pathogens¶ maintain high incidence and

the ability to spread¶ efficiently even as the susceptible host population¶ declines, either through frequency-dependent transmission¶ or the presence of a reservoir host species (de¶ Castro and Bolker 2005). Here, we consider a

less appreciated¶ pathway to host extinction, a disease that¶ spreads rapidly through a tolerant host population¶ followed by host mortality linked to an environmental¶ stressor.

Extinction genetically impossible and empirically disprovenPosner 2005 (Richard A., Judge U.S. Court of Appeals 7th Circuit, Professor Chicago School of Law, January 1, 2005, Skeptic, Altadena, CA, Catastrophe: Risk and Response, http://goliath.ecnext.com/coms2/gi_0199-4150331/Catastrophe-the-dozen-most-significant.html#abstract)

Yet the fact that Homo sapiens has managed to survive every disease to assail it in the 200,000 years or so of its existence is a source of genuine comfort, at least if the focus is on extinction events. There have been enormously destructive plagues , such as the Black Death, smallpox , and now AIDS, but none has come close to

destroying the entire human race. There is a biological reason. Natural selection favors germs of limited lethality ; they are fitter in an evolutionary sense because their genes are more likely to be spread if the germs do not kill their hosts too quickly . The AIDS virus is an example of a lethal virus, wholly natural, that by lying dormant yet infectious in its host for years maximizes its

spread. Yet there is no danger that AIDS will destroy the entire human race. The likelihood of a natural pandemic that would cause the extinction of the human race is probably even less today than in the past (except in prehistoric times, when people lived in small, scattered bands, which would have limited the spread of disease), despite wider human contacts that make it more difficult to localize an infectious disease. The reason is improvements in medical science. But the comfort is a small one. Pandemics can still impose enormous losses and resist prevention and cure: the lesson of the AIDS pandemic. And there is always a lust time. That the human race has not yet been destroyed by germs created or made more lethal by modern science, as distinct from completely natural disease agents such as the flu and AIDS viruses, is even less reassuring. We haven't had these products long enough to be able to infer survivability from our experience with them. A recent study suggests that as immunity to smallpox declines because people am no longer being vaccinated against it, monkeypox may evolve into "a successful human pathogen," (9) yet one that vaccination against smallpox would provide at least some protection against; and even before the discovery of the smallpox vaccine, smallpox did not wipe out the human race. What is new is the possibility that science, bypassing evolution, will enable monkeypox to be "juiced up" through gene splicing into a far more lethal pathogen than smallpox ever was.

Lethal diseases burn out fast—Ebola proves Morse, 4 (Stephen Morse, director of the Center for Public Helth Preparedness, at the Mailman School of Public Health of Columbia University, 04 ActionBioscience.org, “Emerging and Reemerging Infectious Diseases: A Global Problem", 2004, http://www.actionbioscience.org/newfrontiers/morse.html, [Zheng])

ActionBioscience.org: How do infectious diseases become pandemic? Morse: A pandemic is a very big epidemic. It requires a number of things.

There are many infections that get introduced from time to time in the human population and, like Ebola,

burn themselves out because they kill too quickly or they don’t have a way to get from person to person . They are a terrible tragedy, but also, in a sense, it is a lucky thing that they don’t have an efficient means of transmission. In some cases, we may inadvertently create pathways to allow transmission of infections that may be poorly transmissible, for example, spreading HIV through needle sharing, the blood supply, and, of course, initially through the commercial sex trade. The disease is not easily transmitted, but we provided, without realizing it, means for it to spread. It is now pandemic in spite of its relatively inefficient transmission. We also get complacent and do not take steps to prevent its spread.

Diseases won’t cause extinction – humans will outgrow diseaseNational Geographic, 2004 (“Our Friend, The Plague: Can Germs Keep Us Healthy?” September 8, http://www.promedpersonnel.com/whatsnew.asp?intCategoryID=73&intArticleID=443)

Disease organisms can, in fact, become less virulent over time . When it was first recognized in Europe around 1495, syphilis

killed its human hosts within months. The quick progression of the disease – from infection to death – limited the ability of syphilis to spread. So a new form evolved, one that gave carriers years to infect others. For the same reason, the common cold has become less dangerous. Milder strains of the virus – spread by people out and about, touching things, and shaking hands – have an evolutionary advantage over more debilitating strains. You can’t spread a cold very easily if you’re incapable of rolling

out of bed. This process has already weakened all but one virulent strain of malaria : Plasmodium falciparum succeeds in part because bedridden victims of the disease are more vulnerable to mosquitoes that carry and transmit the parasite. To mitigate malaria, the secret is to improve housing conditions. If people put screens on doors and windows, and use bed nets, it creates an evolutionary incentive for Plasmodium falciparum to become milder and self-limiting. Immobilized people protected by nets and screens can’t easily spread the parasite, so evolution would favor forms that let infected people walk around and get bitten by mosquitoes. There are also a few high-tech tricks for nudging microbes in the right evolutionary direction. One company, called MedImmune, has created a flu vaccine using a modified influenza virus that thrives at 77 degrees Fahrenheit instead of 98.6 degrees Fahrenheit, the normal human body temperature. The vaccine can be sprayed in a person’s nose, where the virus survives in the cool nasal passages but not in the hot lungs or elsewhere in the body. The

immune system produces antibodies that make the person better prepared for most normal, nasty influenza bugs. Maybe someday we’ll barely notice when we get colonized by disease organisms. We’ll have co-opted them. They’ll be like

in-laws, a little annoying but tolerable. If a friend sees us sniffling, we’ll just say, Oh, it’s nothing – just a touch of the plague.

Virus burnout solves the impactThe Guardian, 2003 (“Second Sight”, September 25, http://technology.guardian.co.uk/online/story/0,3605,1048929,00.html)

The parallel with the natural world is illustrative. Take the case of everyone's favourite evil virus, Ebola . This is so virulent that it kills up to 90% of infected hosts within one to two weeks. There is no known cure. So how come the entire population hasn't dropped dead from haemorrhaging, shock or renal failure? The "organism" is just too deadly: it kills too quickly and has too short an incubation period, so the pool of infected people doesn't grow .

Squo solves whatnotStatus quo solves marine biotechnology to develop antibiotics, but terrestrial resources are more importantBruckner 13—coral reef ecologist in the National Marine Fisheries Service’s Office of Protected

Resources (Andrew W., Silver Spring, Maryland, “Life-Saving Products from Coral Reefs”, Issues in Science and Technology, November 27, 2013, http://issues.org/18-3/p_bruckner/)

Coral reefs are storehouses of genetic resources with vast medicinal potential, but they must be properly managed. During the past decade, marine biotechnology has been applied to the areas of public health and human disease, seafood safety, development of new materials and processes, and marine ecosystem restoration and remediation. Dozens of promising products from marine organisms are being advanced, including a cancer therapy made from algae and a painkiller taken from the venom in cone snails. The antiviral drugs Ara-A and AZT and the anticancer agent Ara-C, developed from extracts of sponges found on a Caribbean reef, were among the earliest modern

medicines obtained from coral reefs. Other products, such as Dolostatin 10, isolated from a sea hare found in the Indian Ocean, are under clinical trials for use in the treatment of breast and liver cancers, tumors, and leukemia. Indeed, coral reefs represent an important and as yet largely untapped source of natural products with enormous potential as pharmaceuticals, nutritional supplements, enzymes, pesticides, cosmetics, and other novel commercial products. The potential importance of coral reefs as a source of life-saving and life-enhancing products, however, is still not well understood by the public or policymakers. But it is a powerful reason for bolstering efforts to protect reefs from degradation and overexploitation and for managing them in sustainable ways. Between 40 and 50 percent of all drugs currently in use, including many of the anti-tumor and anti-infective agents introduced during the

1980s and 1990s, have their origins in natural products. Most of these were derived from terrestrial plants, animals, and microorganisms, but marine biotechnology is rapidly expanding. After all, 80 percent of all life forms on Earth are present only in the oceans. Unique

medicinal properties of coral reef organisms were recognized by Eastern cultures as early as the 14th century, and some species continue to be in high demand for traditional medicines. In China, Japan, and Taiwan, tonics and medicines derived from seahorse extracts are used to treat a wide range of ailments, including sexual disorders, respiratory and circulatory problems, kidney and liver diseases, throat infections, skin ailments, and pain. In recent

decades, scientists using new methods and techniques have intensified the search for valuable chemical compounds and genetic material found in wild marine organisms for the development of new commercial products. Until recently, however, the technology needed to reach remote and deepwater reefs and to commercially develop marine biotechnology products

from organisms occurring in these environments was largely inadequate. The prospect of finding a new drug in the sea, especially among coral reef species, may be 300 to 400 times more likely than

isolating one from a terrestrial ecosystem. Although terrestrial organisms exhibit great species diversity, marine organisms have greater phylogenetic diversity, including several phyla and thousands of species found nowhere else. Coral reefs are home to sessile plants and fungi similar to those found on land, but coral reefs also contain a diverse assemblage of invertebrates such as corals, tunicates, molluscs, bryozoans, sponges, and echinoderms that are absent from terrestrial ecosystems. These animals spend most of their time firmly attached to the reef and cannot escape environmental perturbations, predators, or other stressors. Many engage in a form of chemical warfare, using bioactive compounds to deter predation, fight disease, and prevent overgrowth by fouling and competing organisms. In some animals, toxins are also used to catch their prey. These compounds may be synthesized by the organism or by the endosymbiotic microorganisms that inhabit its tissues, or they are sequestered from food that they eat. Because of their unique structures or properties, these compounds may yield life-saving medicines or other important industrial and agricultural products.

The US is exploring the ocean now for cures of diseasesNOAA no date (NOAA, no date, “Medicines From the Sea”, http://www.noaa.gov/features/economic_0309/medicines.html, 7/1/14, AG)

Ocean exploration often leads to new ideas, new theories and discoveries, including new medicines. From slime to sponges, researchers are exploring the ocean's depths for new medications to treat cancer, bacterial infections, viruses, heart disease, pain, and other ailments.¶ The seas contain an uncounted number of species of plants and animals. These creatures provide a vast storehouse of chemical compounds unknown on

land. An ocean commission report lists chemicals and biological materials from marine organisms now in use or development, including 10 anti-cancer drugs, drugs to fight inflammation, fungus, tuberculosis, HIV, malaria and dengue.

Bioprospecting suxBioprospecting iz badSatel 5

(Sally, MD and lecturer at Yale School of Medicine, Diminishing Biodiverse Returns," Feb 16 2005, http://www.aei.org/article/health/diminishing-biodiverse-returns/

But, in truth, bioprospecting actually constitutes a small and shrinking percentage of the portfolio of major drug companies. Eli Lilly, for example, has not engaged in the activity for several years. It is high risk and very low yield. Instead, companies screen millions of synthetic molecules for promising medicinal leads. Natural molecules, it turns out, are often maddeningly intricate and thus it is hard to replicate the molecular structure reliably and to reproduce the substance on a large scale for manufacturing. Japanese pharmaceutical companies, for example, have had virtually no success in isolating key elements from traditional herbal medicines and commercializing drugs from them.

AT Antibiotic ResistanceCurrent treatment effectively curtails resistant bacteria growthMorran 13 1/15/2013-PHD, NIH postdoctoral fellow at Indiana University, research recently featured on BBC (Levi, “Averting the Approaching Apocalypse,” Nothing In Biology.org, http://nothinginbiology.org/2013/01/15/averting-the-approaching-apocalypse/)

A paper by Quan-Guo Zhang and Angus Buckling (2012) takes an experimental evolution approach to begin addressing this issue empirically. In search of a different strategy for curbing the evolution of antibiotic resistance in their experimental populations of the bacterial species

Pseudomons flourences, Zhang and Buckling treated their bacterial populations with either antibiotics, a bacteriophage or “phage” (a virus that attacks bacteria), or a combination of the antibiotic and phage. Zhang and Buckling predicted that the combination treatment

might be more effective than either antibiotics or phage alone because the combination treatments should better reduce bacterial population sizes and limit their response to selection (Alisky et al. 1998, Chanishvili 2001, Comeau

2007). Additionally, bacterial mutations that confer resistance to antibiotics generally do not also confer resistance to phage, so evolution of resistance to the combination treatments would likely require at least two mutations, and thus require more time to evolve resistance than the other treatments (Chanishvili 2001, Kutateladze 2010). Zhang and Buckling evolved their bacterial populations under the 3 different treatments (in

addition to a control in which they allowed the bacterial populations to grow under normal conditions) for 24 days. A total of 24 replicate populations were exposed to each treatment. After 24 days of bacterial evolution none of

the replicate populations exposed to control conditions or phage went extinct (Figure 1). In contrast, 12 of the replicate populations exposed to only the antibiotic were extinct while 23 of the populations exposed to combination treatment went extinct (Figure 1).

Therefore, the combination treatment was the most effective treatment for killing the bacteria. However, that single population that survived the combination treatment could mean trouble. Intense natural selection, like that imposed by the combination treatment, could have produced a super-strain of the bacteria. Creation of a super-strain, in this case a strain resistant to both the antibiotic and phage with little cost of maintaining such resistance,

would be troubling because the antibiotic-phage combination treatment strategy would have only accelerated the arms race rather than curbing it. However, in many cases the evolution of resistance comes with fitness costs, like significantly reduced growth rates in absence of the antibiotic or phage. These fitness costs are thought to stop the spread of some antibiotic resistant strains simply because the strains cannot successful compete with strains in nature when the antibiotic is not present. Zhang and Buckling tested the fitness of their surviving populations in competition with the ancestral bacterial population that represents the starting point for evolution in this experiment. They found that in a short term loans scenario, only the control bacteria increased in fitness relative to the ancestor when competed under control conditions (Figure 2). More importantly, they observed that the fitness of the single surviving population from the combination treatment was less

than half of the ancestor’s fitness in the absence of antibiotic and phage (Figure 2). Therefore, the antibiotic plus phage treatment resulted in the extinction of 23 out of 24 bacterial replicate populations, while the lone surviving population was far from being a super-strain. The ability of the surviving bacterial populations to grow under normal conditions was assessed relative to their ancestral bacterial population. Here, any deviation from 0 is indicative of evolutionary

change (a change from the ancestor population). Control populations increased in fitness under normal growth conditions, while populations exposed to either phage or antibiotic exhibited reduced fitness. Most importantly, the population that survived the combined treatment of antibiotic and phage evolved greatly reduced fitness under normal conditions (Zhang and Buckling 2012).

No major impacts from anti-biotic resistanceUrrutia 2014 -a PhD candidate in Health Policy, Ethics Concentration, at Harvard University, holds a BA in Philosophy, Politics, and Economics from the University of Pennsylvania (Julián, “The bright side of antibiotic resistance,” Harvard Law, http://blogs.law.harvard.edu/billofhealth/2014/02/07/the-bright-side-of-antibiotic-resistance/)

But bacteria don’t care. They’re (still) here, they’re (always) evolving, get used to it. I say that because I don’t believe we’re going to be able to keep discovering new classes of antibiotics ad infinitum–although I certainly hope I’m wrong. But if I’m not, it means that we’re only ever going to have so many treatment options, and that the bugs are eventually going to become resistant to all of them (although probably not in our lifetime). What then? And what do we do until then? Let’s start with the first one, since post-apocalyptic scenarios are always fun: Medicine will certainly have to change.

Hospitals will become very, very dangerous places (much more than they already are!)… There’s going to be much stronger and urgent pressure to reduce hospital stays and readmissions to the absolute minimum, and most patient care will have to be shifted to community and home settings…. Health systems will have to go through major structural transformations to improve prevention…. GP’s, primary-care specialists, and allied healthcare professionals will become much more important and esteemed members of the healthcare professions…. The notion that

individual health is highly interdependent will become a part of popular culture. Funny–apart from the first part about hospitals becoming (more)

dangerous, none of these sound all that terrible. In fact, they’re all changes I would very much like to see in my lifetime, bacterial apocalypse or not. It sounds like we would save a lot of lives, avoid a lot of suffering, and spend a lot less money doing it. It certainly makes me wonder why we aren’t doing a lot of those post-apocalyptic things now (i.e. way before the apocalypse.) We should probably also be trying harder to prevent resistance, even if it does happen to be true that it’s battle we will eventually lose. For example, we should

make a bigger effort to identify “germ sheds” and bacterial “breeding grounds,” and we should be making an even bigger effort to eliminate them. (One would think that the imperative to eliminate them is an obvious corollary of the imperative to identify them, but we’ve known for a long time that overcrowded prisons are a major source of super-bugs, and yet we still seem quite pleased to have overcrowded prisons proliferating… I guess corollaries just aren’t very popular nowadays.) However, the idea that we will not be able to keep our drugs effective forever suggests that there are certain things we should not be doing in the name of “stewardship.” For example, we should not withhold antibiotics from patients for whom they are currently a life-saving or suffering-ending option simply because doing so might save/help other patients tomorrow. (Again, to me this seems like a line out of “Deep Thoughts by Captain Obvious,” but millions are currently dying from lack of access to antibiotics that are still effective for their conditions, and I suspect that “stewardship” could become a way of justifying that.) To summarize:

Antibiotic resistance is a scary thing. Last summer I would probably have lost a loved one due to a ruptured appendix (i.e. due to a failure of early detection, which is part of primary care). Peritonitis is a serious condition even

now, but it would most likely have been fatal if the bugs that hit her had been resistant to the antibiotics we have available. I don’t like antibiotic resistance one bit. But at least it serves to remind us that there are better approaches to healthcare that could be realized within our lifetime, and at least it does not give us any reason to deny each other proper care and consideration if we happen to get sick today.

AT Tuberculosis

New Drugs SolveNew vaccines solveVaccine Weekly 9 (1/21, "Tuberculosis; Sequella lead drug compund SQ109 selected for phase 1B clinical trial program", 1-21, p.85, ProQuest,

2009 JAN 21 - (<http://www.newsrx.com> NewsRx.com) -- Sequella, Inc., a clinical-stage biopharmaceutical company focused

on diseases of epidemic potential, announced that SQ109, its lead drug candidate for the treatment of tuberculosis (TB), was the first drug approved for evaluation in a newly awarded clinical program contract to Dynport Vaccine

Company LLC and Quintiles Transnational. The contract, awarded by the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), is part of NIAID's clinical resource infrastructure to accelerate Phase 1

studies of promising clinical stage drugs or vaccines that address emerging and re- emerging infectious tropical diseases and bioweapon pathogens. The Phase 1B clinical study of SQ109 should be initiated in Q1 2009 (see also <http:// www.newsrx.com/library/topics/Tuberculosis.html> Tuberculosis). SQ-109 is a new diamine antibiotic intended to replace one or more of the

current first-line anti-TB drugs and simplify patient therapy. SQ109 was granted U.S. FDA Fast Track designation and

FDA/EMEA Orphan Drug Designation in 2007. SQ109 shows activity against drug sensitive and multi-drug resistant

(MDR and XDR) Mycobacterium tuberculosis, the causative agent of TB. The Phase 1B study will assess safety and pharmacokinetics of multiple doses of SQ109 in healthy subjects. "This is absolutely the best of both worlds for Sequella," commented Dr. Carol Nacy, Sequella CEO. "We again successfully competed for support from our most valued funding partner, NIAID, while retaining the capacity to work with the same industry-leading contract research organization, Quintiles Transnational, that conducted our first-in-human Phase 1A trial for SQ109.

And, new drugs overcome the factors that cause resistance.AIDS Weekly 9 ("HIV/AIDS Co-Infection; Beating the Number-One Killer in AIDS: Tuberculosis", p.72, 1-1, ProQuest)

Researchers from PolyMedix and the University of Pennsylvania reported their findings in a poster, "Antimicrobial

Molecules for Treatment of Multi-drug Resistant (MDR) and Extensively Drug Resistant (XDR) Strains of Mycobacterium Tuberculosis," at the HIV DART conference on antiretroviral therapies, held in Puerto Rico December 9-12, 2008. Investigators screened a library of PolyMedix's HDP mimics in collaboration with the Tuberculosis Antimicrobial Acquisition Facility, a

branch of the National Institute of Allergy and Infectious Diseases. Three of the antimicrobial compounds exhibited high antimicrobial activity (IC90 < 5 g/ml) against H37Rv, a common laboratory strain of M. tuberculosis, with selectivity greater than

30-120 fold for TB versus mammalian cells. Because they have a biophysical mechanism of action, and do not operate through known biological pathways or specific molecular targets, PolyMedix's HDP mimics are unlikely to cause antimicrobial resistance -- the mechanism by which antibiotic drugs lose their effectiveness over time. PolyMedix has confirmed the lack of experimental resistance to these and other of its HDP mimic antibiotic compounds against a wide range of infectious agents through "serial passaging" studies. These tests involve re-culturing the infective organism, grown in the presence of the drug, for many generations. No increase in minimum inhibitory concentration has been noted for any bacterium paired with a PolyMedix HDP mimic compound.

Status quo vaccinations solve Landry and Heilman 5 (Sarah Landry and Carole Heilman, the associate director of policy and program operations, National Vaccine Program Office, U.S. Department of Health and Human Services, and director of the Division of Microbiology and Infectious Diseases at the National Institute of Allergy and Infectious Disease, Future Directions In Vaccines: The Payoffs Of Basic Research, May 2005, http://web.lexis-nexis.com.fetch.mhsl.uab.edu/universe/document?_m=51cf6e9a7f9bd548830ee047df23ba89&_docnum=4&wchp=dGLzVlz-zSkVb&_md5=d4451074a68f45367fedda32084e521c)

Promise of new technologies. The payoffs from these standard approaches are now beginning to plateau. In fact, most of the "easy" vaccines have been developed, and many challenges lie ahead for new and improved vaccines.

New technologies may provide stronger, broader, and more durable immune responses than those induced by some earlier vaccines. New vaccines are also likely to exploit genomics and high-throughput screening approaches that are based on computational methods. These methods will allow for

development of rationally based approaches that select potential antigens more effectively and precisely. In addition, future vaccines will use these new tools to get around the challenges of the remaining infectious diseases. [n2] These challenges include the inherent ability of many viruses to change (antigenic variation),

as is seen with HIV and influenza; the need to develop vaccines that rely on cell-based immunity for protection for infections such as tuberculosis; and tools for addressing a pathogen's ability to outsmart the immune system--immune evasion strategies, such as seen with hepatitis C. [n3] Impact of new immune concepts. Research on the immune system has helped identify new ways of fighting infections and is helping define the mechanisms needed for successful immunization. Most currently licensed vaccines protect by producing neutralizing antibodies, made by the B cells of the immune system. One of the advantages of stimulating this arm of the

immune system is that it can be easily measured. Researchers believe that vaccines against many of the infections that are of highest priority (HIV, TB, and malaria) will need to have the other arm of the immune system--the cellular component, or T cells--pulled into action. [n4] For the first time in sixty years, new TB vaccines are in clinical trials. [n5]

No Resistant Strains No such thing as incurable strains—Peru study proves.News Rx 8 (8/18, "Harvard Medical School; Comprehensive treatment of extensively drug-resistant TB works, study finds", p.2467, 8-18, ProQuest)

The death sentence that too often accompanies a diagnosis of extensively drug- resistant tuberculosis (XDR-TB) can be commuted if an individualized outpatient therapy program is followed -- even in countries with limited resources and a heavy burden of TB. A study conducted in Peru between 1999 and 2002 shows that more than 60 percent of XDR-TB patients not co-infected with HIV were cured after receiving the bulk of their personalized treatment at home or in community-based settings. The paper appears in the August 7, 2008 issue of The New England Journal of Medicine. "It's essential that the world know that XDR-TB is not a death sentence," says lead author Carole Mitnick, instructor in the Department of Global Health and Social Medicine

at Harvard Medical School (HMS). "As or even more importantly, our study shows that effective treatment does not require hospitalization or indefinite confinement of patients." In some parts of the world, however, patients with XDR-TB and other drug- resistant forms of the disease are confined against their will in TB hospitals that resemble prisons, Mitnick adds. Researchers from HMS, Brigham and Women's Hospital, Partners In Health, Harvard School of Public Health, and the Massachusetts State Laboratory Institute, along with Lima, Peru-based organizations Socios

en Salud, the Peruvian Ministry of Health, and Hospital Nacional Sergio E. Bernales, had already demonstrated that aggressive, outpatient treatment could cure multi-drug resistant tuberculosis (MDR-TB), which is resistant to two first-line anti-TB drugs. That pilot program has been adopted as a national endeavor by the Peruvian government. A similar protocol was used for the recent study of XDR-TB, which is caused by TB bacteria that are resistant not only to the same first-line anti-TB drugs, but also to the two most important second-line drug classes.

No ImpactNo risk of spreadingCollins and Fidel 7 (Lois M. Collins and Steve Fidel Deseret Morning News June 3, 2007 Sunday) http://web.lexis-nexis.com/universe/document?_m=f074682274f46d461ed74eb44d822c9a&_docnum=17&wchp=dGLbVzb-zSkVA&_md5=3d7b5016a80a5dee75c1b63bd175e216

The frenzy over tuberculosis spawned by a single "extensively drug-resistant" case is capturing headlines. But most people exposed to the airborne bacteria will never develop active disease. The Atlanta attorney's case has health officials concerned because his TB falls into a class of infections that resists two first-line TB drugs and some second-line drugs -- one of only 49 other extensively drug-resistant cases reported in the United States between 1993 and 2006. There's also a class

called multidrug-resistant TB, which is easier to treat than cases like this one but more difficult than typical TB. Although it's harder to kill, it's no easier to spread than any other tubercolosis, according to Carrie Taylor, an infection control practice nurse at LDS Hospital. "You have to breathe in air that's coughed." Doctors treat an average of 38 active TB cases each year in Utah, according to the Utah Department of Health. The disease usually settles in the lungs, although it can affect the kidneys, spine, brain and other organs. The disease is caused by Mycobacterium tuberculosis, which spreads person-to-person but only through close contact. Taylor and her colleague Vickie Anderson, also an infectn-control practice nurse at LDS Hospital, describe it as passing from one person's lungs directly into another's. It's not like a cold that is easily spread and fairly hardy. In fact, sunlight kills it. Unless the individual has a drug-resistant TB strain -- "not common in Utah," said Taylor -- it's very treatable, although it takes a long time and several medications. Left untreated, it can kill. At least initially, patients are isolated to avoid spread of the disease. Both chicken pox and measles are more contagious, said infectious disease specialist Dr. John Kriesel of University Hospital. As an example, when a Provo High School student was recently diagnosed with tuberculosis and health officials asked 250 of the student's school contacts to be tested for it, Kriesel predicted "not one of them will test

positive for TB." People in casual contact are extremely unlikely to get the disease. Just being exposed doesn't mean you could pass it on, Taylor said. Without symptoms, you can't spread it, even if you have a positive skin test. People who live with a patient are at higher risk, but most won't get it, either.

Alt CausesNo global solvency, TB is in 90 countriesShah et al 7 (N. Sarita Shaw, CDC and WHO, Abigail Wright, Gill-Han Bai, Lucia Barrera, Fadila Boulahlbal, 15 other epidemiology experts, Emerging Infectious Diseases, 13:3, March, "Worldwide emergence of extensively drug-resistant tuberculosis", http://origin.cdc.gov/eid/content/13/3/pdfs/380.pdf)

Multidrug-resistant tuberculosis (MDR TB) has been documented in nearly 90 countries and regions worldwide (1); 424,203 cases of MDR TB were estimated to have occurred in 2004, which is 4.3% of all new and previously treated TB cases (2). Treatment for MDR TB

patients requires use of second-line drugs for >24 months. These drugs are more costly, toxic, and less effective than first-line drugs used for routine treatment of TB (3–6). As with other diseases, resistance to TB drugs results primarily from nonadherence by patients, incorrect drug prescribing by providers, poor quality

drugs, or erratic supply of drugs (7).

Russia outweighsZuger 2k (Abigail, New York Times, "Russia has few weapons as infectious diseases surge", 12-5, L/N)

But this is Russia, where TB, once nearly under control, has become epidemic since the collapse of the Soviet Un-ion. Doctors often use air injections to fight TB strains that resist the most commonly used drugs. The technique com-presses infected lungs, giving them time to rest and heal. Ms. Kostina, 24, was healthy until two years ago, working as a nurse at the local prison, just a mile down the road from this hospital. There, as in most of Russia's overcrowded prisons, tuberculosis has been spiraling out of control . When she fell ill with fever and a cough, doctors quickly ascertained that she had caught tuberculosis

from one of her inmate patients. Despite months of treatment, her disease got worse. All four of the antituberculosis drugs she tried were powerless against it. Moreover, during the year she spent traveling from work to home, then into the hospital, then to a convales-cent home, then

back to the hospital, she had undoubtedly exposed dozens of others to her drug-resistant germs. Russia's political turmoil, its economic crisis and its new freedoms have been accompanied by a wave of old dis-eases. Tuberculosis is flooding the country, producing what some authorities are calling the world's largest outbreak of the drug-resistant variety, one of medicine's most ominous problems. Rates of other infections, including hepatitis, syphilis and AIDS, are skyrocketing. An epidemic of diphtheria swept

through in the mid-1990's. Reports of smaller, regional outbreaks of encephalitis, typhoid fever, malaria, polio, pneu-monia and influenza pepper the nightly news. Health experts describe Russia's prison system as an "epidemiologic pump," continuously seeding the country with pockets of tuberculosis that can spread on their own. Increasingly, TB cases of Russian origin are turning up in the Bal-tic countries and even farther afield -- for instance, Germany and Israel. Specialists worry that if the rising rates of infectious diseases in Russia continue unabated, the country itself may turn into an epidemiologic pump, sending infectious diseases into the rest of the world. "It's not surprising to see a case here," said Barry N. Kreiswirth, a tuberculosis expert at the Public Health Research Institute in New York City, "but it's a good reminder that it doesn't take

much for one person to be a vector and start an epidemic."

Poverty root cause—not vice versaCohen 1 – former director of the United Nations Development Programmes HIV and Development program and Senior Advisor to the UNPD on HIV and Development-2001 ( Desmond Cohen, "Poverty and HIV/AIDS in Sub-Saharan Africa," Issue NO.27, http://www.undp.org/hiv/publications/issues/english/issue27e.html)

There are also the direct effects of what has happened to the children which are material and damaging to their futures. Poor nutrition leads to poor health which is an important cause of low labour productivity and thus the

persistence of low incomes for the poor. Poor and damp housing is a major factor in causing illnesses such as TB which is itself exacerbated by the HIV epidemic (where there is now a dual epidemic underway in Africa). These children will continue to experience poor health status over their lifetimes with all kinds of social and economic consequences for them and their families.

Alt cause, HIVIPS 9 (Inter Press Service, AllAfrica, "Zimbabwe; doctors fear high risk of drug-resistant TB", 3-3,L/N)

Someone in the world is newly infected with tuberculosis (TB) bacilli every second; overall, one-third of the world's population is currently infected with the TB bacillus. TB is spread through the air when infectious people cough, sneeze, talk or spit, they propel TB germs, known as

bacilli, into the air. A person needs only to inhale a small number of these to be infected. Left untreated, each person with active TB disease will infect on average between 10 and 15 people every year. But people infected with TB bacilli will not necessarily become sick with the disease. The immune system "walls off" the TB bacilli which, protected by a thick waxy coat, can lie dormant for years. HIV and TB form a lethal combination, each speeding the other's progress. HIV weakens the immune system; someone who is HIV-positive and infected with TB bacilli is many times more likely to become sick with TB. TB is a leading cause of death among people who are HIV-positive. In Africa, HIV is the single most important factor contributing to the increase in incidence of TB since 1990.

Russian TB outweighs US TBFeschbach and Keshavjee 7 - *instructor at Bringham and Women's Hospital at the Harvard Medical School, **Senior Scholar at the Woodrow Wilson Center ("Drug-Resistant TB in Russia", Woodrow Wilson International Center for Scholars, 7-24, http://www.wilsoncenter.org/index.cfm?topic_id=116811&fuseaction=topics.event_summary&event_id=239772,)

It is expected that 62 percent of all new multidrug-resistant tuberculosis (MDR-TB) cases will be concentrated in Russia, China, and India, warned Dr. Salmaan Keshavjee, instructor at the Brigham and Woman's Hospital and Harvard Medical School. Speaking at a July 24, 2007

discussion co-sponsored by the Global Health Initiative and the Kennan Institute, Dr. Keshavjee said that although people have known for a number of years that mycobacterium tuberculosis

(TB) is prone to resistance when treated ineffectively, overall, the number of antibiotic-resistant strains of TB

continues to rise. Some experts worry that a ‘perfect storm’ of HIV, very high TB rates, and a programmatic infrastructure that lacks the ability to adequately address complex health interventions is brewing in the former Soviet republics, he continued. Murray Feshbach, senior scholar at the Woodrow Wilson Center, highlighted the lethargy in addressing TB in Russia by mentioning that, until quite recently, political will and funding were not available in substantial levels to address the health crisis facing the Russian population. Based on his research and first-hand experience,

Russian officials have been extremely slow to address TB at the national level, and are just now beginning to acknowledge the existence of extensively drug-resistant tuberculosis (XDR-TB)

within the Russian population. The substantial success in controlling TB during the Soviet years has been lost, and TB deaths have skyrocketed in Russia over the past 18 years, particularly among working-age men. Much of this increase is due to overcrowding in urban centers, and in prison populations especially, explained Dr. Keshavjee. Globally, TB strains—including MDR- and XDR-TB strains—kill approximately 1.8 million people per

year, he said, disproportionally affecting the poor and immunocompromised.

Uncoordinated testing makes resistant TB inevitable.The Lancet 9 (“Crunch time for tuberculosis control", 373:9670, p. 1145, 4-4, ProQuest)

In 2007, there were 9.3 million incident reports of tuber culosis ; half in Asia and a third in Africa. Overall, 1.3 million people were co-infected with HIV. 456 000 co-infected individuals died, making tuberculosis the commonest cause of death in people with HIV/ AIDS. Conversely, HIV/AIDS was responsible for almost a quarter of the 1.7 million deaths in people with tuberculosis . 500 000 people were thought to have MDR-TB and perhaps another 40 000 to have XDR-TB.

India and China have the world's largest burdens of incident tuberculosis, 2.0 million and 1.3 million people, respectively, and both have over 100 000 people with MDR-TB. The tragedy-some might say folly-is that established procedures for HIV/AIDS co-infection and MDR-TB have not been implemented widely. In 2004, WHO urged more collaboration between HIV

and tuberculosis programmes, with routine testing for HIV in people with tuberculosis and for tuber culosis in people with HIV/AIDS. Testing accelerates diagnosis, improves treatment, and protects immunocompromised with HIV from tuber culosis. However, testing and treatment for the two infections often occur at separate sites. In 2007, the Global Plan targets

for intensified case finding were missed worldwide. In Africa, the aim was to test 900 000 people with tuberculosis for HIV and 13 million people with HIV for tuberculosis. Only 500 000 and 300 000, respectively, were screened-and few of those diagnosed with co-infection received

appropriate treatment. MDR-TB is encouraged by poor case-detection, treatment with inappropriate drug regimens, and lack of clinical supervision. Almost half of treatment relapses in eastern Europe are from drug-resistant strains. Accurate diagnosis of MDR/ XDR-TB requires drug sensitivity testing in a qualified laboratory. Only 2% of the

estimated 500 000 people infected with drug-resistant strains were tested in 2007. And even when diagnosed with this more lethal form of tuberculosis, fewer than 3% received treatment recommended by international guidelines. Mechanisms to ensure best practice have failed at many levels in several countries because of lack of discipline, infrastructure, and resources.

Clearly the changing nature of tuberculosis epidemiology demands a reassessment and scaling-up of

control measures. To redefine and redirect the actions necessary to combat tuberculosis, resolu tions from the Stop TB Partners Forum will be presented in Beijing on April 1-3, when health ministers from the countries most affected by MDR/ XDR-TB will

discuss strategies for tackling drug- resistant infection. To succeed they will need to build consensus, establish political will, and secure sustainable funding.

Drug use makes it inevitableNational Institute of Drug Abuse 6 (National Institute of Drug Abuse, NIDA InforFacts: Drug Abuse and the Link to HIV/AIDS and Other Infectious Diseases, "HIV/AIDS," December 2006, http://www.nida.nih.gov/Infofacts/drugabuse.html)

Besides increasing their risk of HIV infection, individuals who take drugs or engage in high-risk behaviors associated with drug use also put themselves and others at risk for contracting or transmitting hepatitis C (HCV), hepatitis B (HBV), tuberculosis (TB), as well as a number of other sexually transmitted diseases, including syphilis, chlamydia,

trichomoniasis, gonorrhea, and genital herpes. Injecting drug users (IDUs) are also commonly susceptible to skin infections at the site of injection and to bacterial and viral infections, such as bacterial pneumonia and endocarditis, which, if left untreated, can lead to serious health problems.

Migration makes TB inevitable.Chest Medicine 7 ("The changing face of tuberculosis: a new challenge to the developing world." http://www.priory.com/cmol/tbanga.htm, accessed July 24 2007)

Immigration: the developed world's problem Within the developed world immigration is the greatest factor contributing to the increase in cases. In England 60% of cases are in ethnic minority groups, which comprise only 5% of the population. Of these individuals from the Indian Subcontinent form the majority. For the last two years I have

had no less than two Indian doctors on treatment for TB at any time. In should however, be remembered that tuberculosis was a disease which killed one in four people in Western Europe 200 years ago and was effectively

exported to what is now the developing world through trade and Empire building. There is occurring a reimportation of disease with migration for economic or political reasons.7.Within the developing world migration is also playing a part for example refugees from Somalia in Kenya or from Afghanistan in Pakistan.

AT Zoonotic

SQ SolvesZoonotics have been contained if not eliminated due to the restrictions placed on animal trade, vaccines, and quarantines.Torres 99 (Alfonso, D.V.M., M.S., Ph.D., Deputy Administrator, USDA, Animal Plant and Health Inspection Service, Veterinary Services, “International Economic Considerations Concerning Agricultural Diseases and Human Health Costs of Zoonotic Diseases,” Annals of the New York Academy of Sciences 894:80-82)

Animal diseases can negatively affect the number and availability of animals, their productivity, or their appearance. 1 A few centuries ago, animal diseases affected mostly individual owners or herdsmen, but did not have serious consequences on the larger community. A similar event today will not only have a negative impact on the animal owners, but more importantly, will significantly affect the general economy of

the region, the entire nation, even a group of nations. The importance of animal diseases as an element affecting international trade of animals and animal products has reached its full impact level with the recent designation by the World

Trade Organization (WTO) of the International Office of Epizootics (OIE) as the international agency in charge of establishing animal health standards upon which international commerce can institute restrictions to prevent the spread of animal diseases from one nation to another. It is important to point out that while the spread of human diseases around the world is due to the unrestricted movement of people across political boundaries, animal diseases are, for the most part, restricted to defined geographic areas of the world due to the implementation of animal importation requirements, quarantines, animal movement regulations, and by disease control measures that include mass vaccination campaigns and animal depopulation practices. A number of animal diseases have been eradicated from countries or even from continents around the world by aggressive, well-coordinated, long-term animal health campaigns. This is in contrast to the relatively few human diseases successfully eradicated from large areas of the world.

No SolvencyImpact’s inevitable—people are morally opposed to killing animals to stem the spread of the disease.Blancou et al 5 (Jean, former General Director of OEI, Bruno and Albino, “Emerging or re-emerging bacterial zoonoses: factors of emergence, surveillance and control,” Vet. Res., pg 507-522)

The main obstacles that are encountered in the control of bacterial zoonoses are the same as those opposed to the control of any infectious

disease, that is most often finan- cial and human obstacles rather than tech- nical limitations. The financial resources needed to effi- ciently fight against zoonotic agents are not available for all countries. Only the inter- national community’s financial support, could, notably, allow developing countries to organize a proper control of zoonotic dis- eases, but it is rare that this is materialized as a financial gift and mobilization of spe- cific funds, even by well-known interna- tional organizations (such as WHO, FAO, OIE), is limited for such diseases. Due to all these difficulties, many sanitary authorities of these countries have given up the estab- lishment of such prevention programs. Oth- ers manage, with a lot of perseverance, to elaborate complicated multilateral financial arrangements. This allows punctual projects to be realized, but

rarely to establish the long-term prophylaxis plans that they really need. When financial and material problems are supposedly solved, human-related dif- ficulties should not be underestimated. These difficulties can originate within the services in charge of applying the national prophy- laxis plans, when these services are not themselves convinced of the good use of these plans, or when they

do not seem to get specific benefits from it. The obstacles sometimes result from a lack of cooperation between specific professional categories, amongst which figure breeders, as well as livestock brokers or even veterinarians bothered by the application of certain pro- grams of control or the limited incentive given by the health authorities for perform- ing prophylaxis tasks. Finally, the obstacle to such plans may be caused by the active opposition of the public opinion to certain methods of control. This is notably the case for the hostility of some groups to the mass slaughtering of animals during epizootics, or to the use of vaccines issued from genetic engineering. By lack of an appropriate con- sensus, the control of some zoonotic dis- eases may simply be impossible in some countries.

AT “Superbugs”

Threat is Exaggerated Superbugs are a delusion based on a perverse love of panic – the threat is exaggerated – CRE is not as big an issue as posedSepkowitz, 13. Kent Sepkowitz is an infectious-disease specialist in New York City. He writes for The New York Times, Slate, and O magazine. He also writes academic medical articles. “Why I’m Not Worried About Dying From a Superbug, and You Shouldn’t be Either.” March 8, 2013 http://www.thedailybeast.com/articles/2013/03/08/why-i-m-not-worried-about-dying-from-a-superbug-and-you-shouldn-t-be-either.html

Pity the poor public-health official: in the midst of an epidemic, he must adopt a soothing avuncular tone of near-boredom, a “we’ve seen this, not to worry” sort of yawn to calm people who otherwise seem ready to run screaming into the streets. But on the other hand, in this day of sequestered public-health funding, he has to raise a major ruckus about some other problem that

might happen, swearing that the earth may end soon if we don’t wake up now and face the music. The cavalcade of past get-ready-for-the-big-one hits includes drug-resistant TB, avian flu, swine flu, and drug- resistant gonorrhea among others, each introduced with shrill press releases and snapshots of grim faces peering through microscopes. It is no surprise, therefore, to see the CDC roll out the heavy artillery this week by proclaiming the dangers of the latest superbug . This one is ugly for sure, a resistant-to-almost-everything bacteria that preys on the hospitalized patient. Called carbapenem-resistant Enterobacteriaceae, or CRE, to denote the class of antibiotics (carbapenems) to which it is resistant, and the group of bacterial organisms—Enterobacteriaceae, bacteria that reside in the gut—to which it belongs, CRE is being seen increasingly in hospitals across the U.S. Unheard of before 2001, CRE now is in 181 (4.6 percent) U.S. acute-care hospitals, affecting hundreds of patients. In August 2012, the

NIH Clinical Center had a widely reported outbreak from a CRE that killed six of 18 patients, the mortality rate seen in most series. The CDC and other public-health officials are particularly alarmed by this latest wrinkle because the carbapenem class was the last thoroughly modern group of antibiotics with predictable activity against gut bacteria. With the carbapenem hegemony now wobbling, the next (and last) antibiotic is an oldie from the 1960s, pulled from the market then because of concerns about toxicity, but now being used in many hospitals and ICUs to treat CRE infection. If and when CRE becomes resistant to this old-timer, the cupboard is truly bare. This sort of progressive resistance to antibiotics is standard operating procedure for bacteria exposed to high doses of potent antibiotics over time; resistance can and must occur according to the most basic principle of evolution: survival of the fittest. If a billion bacteria are exposed to an antibiotic and just one bacterium, because of a chance mutation, is resistant to the antibiotic while the other near-billion are not, that single organism will survive while the others will die off. The resistant organism will then have the run of the place with enough nutrition

to support the billion now-absented brethren, allowing the resistant clone to take root and get in position to spread. We have been here before of course: methicillin-resistant Staphylococcus aureus (MRSA) played through the hospitals and the headlines (and even the National Football League ) last decade, alarming the public and spurring new regulations to contain it as well as the application of money, sort of, to develop new weapons. Perhaps because of all the hubbub, MRSA now seems almost quaint and surely not a headline-screaming scourge: mostly contained, a nuisance, a problem, but being dealt with at the right place by the right people. In other words, it has assumed its proper proportion in the world of threats and dangers. The same likely will happen with CRE. More

cases will occur, hospitals will make the necessary adjustments suggested by the CDC, specialists will learn their way around the diseases, and eventually the threat and the excitement around

it will flatten out. And then the next red-hot development on some other front will emerge rendering the acronym to oblivion. The problem though is this: the mix of steady CDC concern about a real issue that requires attention, a world with infinite capacity for both news and “news,” and a perverse public enjoyment of being frightened has succeeded in little other than scaring the crap out of people who might need medical care. Indeed, hospitals seem to occupy the same imagined place as the Overlook Hotel, the cavernous inn Jack Nicholson prowled in The Shining—the last place on earth a sane person would go. Health care in general and hospitals specifically are viewed these days by just about everyone as a veritable killing field , the place where the two inevitabilities—death and taxes—meet daily as people are fleeced then killed. Such is not the case. Honest. Yes, I know I am tainted goods because of my conflict of interest: I work in a hospital and I believe in medical care. But please remember that people in ICUs, where CRE and so many other deadly infections lurk, are not denizens of executive suites. They are already quite ill, usually with multiorgan failure from the heart attack or stroke or high-speed automobile crash that brought them to emergency medical care. They then are exposed to the high-tech ballet of life-sustaining futuristic machines, venous and urinary catheters, potent and often toxic medications, and all the rest. They also are exposed to the bacteria in their own intestines, mouth, and skin, as well those in the environment, much less the imperfectly cleaned hands of

hospital staff. Horrible, heartbreaking, and fully preventable things happen in ICUs, but so too are many lives saved. The demonization of health care has

occurred simultaneously with our deepening fascination of the promise of tomorrow, an almost religious belief that medicine is just inches away from conquering just about everything. These two fantastic extremes pervert reality with equal force and fully obscure the truth about medical care in 2013: we are neither in a hell of ineptitude and willful neglect nor just inches from the next great golden age of health. And though hospitals are complicated, difficult places to spend time, the view that, to preserve health, it is safer to avoid care than to seek it is a dangerous and troubling delusion.

Superbugs aren’t as serious as the population assumes.Sermonis 7 (Nathan Sermonis is a writer for the Cornell Daily Sun. “Gannett:No Need for Outcry Over ‘Super Bug’” http://cornellsun.com/node/25491)

A recent series of deadly methicillin-resistant staphylococcus aureus infections — the “super bug” — have driven the nation into a panic, but some health officials are saying this widespread fear is a severe overreaction. “It’s not a threat to the average person. It can cause minor to serious cases only under specific circumstances,” said Claire Pospisil, spokesperson for the New York State Department of Health .

This specific staph-infection causing bacteria strain, identified over 40 years ago, typically occurs in healthcare settings, but recent media coverage has emphasized dangers posed to the general population from community-associated MRSA which is spread by poor hygiene and close personal contact. Stories of high school and college students becoming severely ill, in some cases even dying, from MRSA have forced many people to think seriously

about the potential dangers posed by the bacteria and take precautions against it. However, according to Sharon Dittman, associate director of community relations at Gannett, many of the concerns erupting from this coverage and drastic prevention measures being taken — closing schools, canceling sports events, disinfecting entire facilities top to bottom — are out of proportion with the real problem. “This has really scared people into making decisions that may or may not be called for,” she said. While she encouraged people to take precautions against the bacteria, like washing hands and not sharing personal items such as razors andtowels, Dittman said the potential risk for developing a serious MRSA infection is quite low, even for collegestudents living in close-quarters conditions. Usually present as a mild skin condition, MRSA infections appear as reddened skin rashes that may develop into boils

or pimples, causing fevers and pain. Pospisil said that at this stage, the infection is not serious as long as it is taken care of. She said, “I think for community-associated MRSA cases, the important thing for people to know is if they have a skin infection, they should have a doctor look at it. The sooner they identify it, the better.” Although the MRSA strain is resistant to methicillin, an antibiotic in the same family as penicillin, infection is treatable. According to Christine Pearson, spokesperson for the Centers for Disease Control and Prevention, these cases can easily be taken care of and are no cause for alarm. “Most MRSA skin infections are mild and don’t cause death,” she said.

Blaming a misinterpretation of a recent CDC report that found 19,000 people died in 2005 from the antibiotic-resistant bacteria, Pearson said the nation has become overly concerned with MRSA. The study indicated that invasive MRSA cases are a serious problem in hospitals and healthcare clinics, but did not indicate heightened risks for most of the general population. “There are two different things here,” she said. According to the CDC, invasive MRSA cases often cause serious complications by infecting bloodstreams and spreading throughout the body, but the more common MRSA skin infections usually do not become this serious. Different people are susceptible to different stages of MRSA infection. Healthy individuals with infections can typically isolate the problem and easily

treat it. On the other hand, people with weak immune systems run a higher risk of developing a case of the potentially deadly invasive MRSA. While health officials across the country are making attempts to calm down frantic parents and students, many welcome the opportunity to educate people on how to avoid MRSA infections, issuing guidelines and fact sheets about the bacteria. Pearson said, “It never hurts to remind people about how to stay safe.” Finding a positive side to the recent nationwide media attention, Dittman said that at least those who do run the risk of developing a life-threatening infection from MRSA will now be aware of the condition. Crediting the CDC report, she said she thinks people will be more likely to understand just how deadly MRSA can be under certain conditions and take the necessary precautions.

Antimicrobiotics Solves

Antimicrobiotics solveScienceDaily 11 (6/17, http://www.sciencedaily.com/releases/2011/06/110616193740.htm, KF)

ScienceDaily (June 17, 2011) — "Super bugs," which can cause wide-spread disease and may be resistant to most, if not all, conventional

antibiotics, still have their weaknesses. A team of Canadian scientists discovered that specific mixtures of antimicrobial agents presented in lipid (fatty) mixtures can significantly boost the effectiveness of those agents to kill the resistant bacteria. This discovery was published online in The FASEB Journal. According to a researcher involved in the study, Richard Epand, Ph.D.

from the Department of Biochemistry and Biomedical Science at McMaster University in Hamilton, Ontario, Canada, "This study may contribute to overcoming the lethal effects of drug resistant bacteria that is becoming an increasing clinical problem, particularly in hospitals."

New Tech Solves The end of illness is closer than we think—medicine advancing fastSiegel-Itzkovich, 13 Judy Siegel-Itzkovich Is the health and science editor at the Jerusalem Post. “The End of Illness” 6/08/2013 http://www.jpost.com/Health-and-Science/The-end-of-illness-315870)After myriad clinical studies on how to prevent disease, there are clear guidelines on what people generally need to do and eat to have a shot a longevity. Yet, from time to time, recommendations fall to the wayside as new

discoveries result in “course corrections” on the path to long life and health. Gobbling multivitamins, for example, is now out and working out in the morning following by a day of office work is out. Prof. David Agus, a prominent 48-yearold oncologist at Cedars-Sinai Medical Center in Los Angeles and author of the bestselling book The End of Illness, has aimed beyond increasing the numbers of nonagenarians around the world. He dispenses medical advice aimed at helping people to live robustly until their last breath – like Moses the prophet was gathered unto his fathers without first suffering from any debilitating illness .

Originally published in 2011 in English by the Free Press Division of Simon and Schuster, the book has just been translated into Hebrew by Matar. (One hopes that the Hebrew edition will expunge the original endorsement that appears on the English version from Lance Armstrong, the disgraced “seven-time Tour de France winner.”) Agus, who comes from a prominent Jewish family – his grandfather, Rabbi Jacob Agus, was a theologian and the author of

books on Jewish history and philosophy – is coming to Jerusalem later this month. The author was invited to attend the Presidential Conference by President Shimon Peres – who is well known for his own healthy longevity. Agus graduated from Princeton University and received his medical degree from the University of Pennsylvania School of Medicine. He then did his residency at Baltimore’s Johns Hopkins Hospital and completed his oncology fellowship training at New York’s famed Memorial Sloan-Kettering Cancer Center, where he also headed the tumor biology lab. His dealings with cancer led to his exploration of genetic influences and his co-founding of two California companies – Navigenics, a personal genetic testing company, and Applied Proteomics, which searches the blood for biomarkers that provide early warning or prevention of disease. Agus us currently a professor of medicine and engineering at the University of Southern California’s Keck School of Medicine. The 335-pageThe End of Illness, his first book, was on The New York Times bestseller

list. At the outset, Agus notes that colleagues were surprised he went to treating and researching cancer because, with exceptions, “there’s little hope for survival in many cases, and the cure is as evasive today as it ever was. I’m infuriated by the statistics, disappointed in the progress that the medical profession has made and exasperated by the backward thinking that science continues to espouse, which no doubt cripples our hunt for the magic bullet.” He continues: “The war on cancer might be ugly and destructive on many levels. But on a positive note there are many lessons learned in the experience of this war that can then be used to prevent future wars and maximize peace .

After all, the goal should be to avoid ever having to go to war rather than to win a war. And in the health realm, this is especially true.” HIS IDEAL end of life is “to live robustly to a ripe old age of 100 or more. Then, as if your master switch clicked off, your body just goes kaput. You die peacefully in your sleep after your last dance that evening. You don’t die of any particular illness, and you haven’t gradually been wasting away under the spell of some awful, enfeebling disease that began years or decades earlier.” The “end of illness,” he writes, “is closer than you might think.”

Protective measures are already in place to stop the spread of Super Bugs. Churchill 7, Bernard M. Churchill is the Chairman in Pediatric Urology at Mattel Children’s Hospital UCLA. “Superbug are dangerous, but we are not powerless against them.” November 7, 2007. http://online.wsj.com/article/SB119439254844384511.html)

Regarding the recent article " Attack of the Superbugs " (Scott Gottlieb, op-ed, Oct. 30), it is correct to point out that the Food and Drug Administration is largely to blame for the lack of new antibiotics against superbugs such as methicillin-resistant staphylococcus aureus (MRSA). But Dr. Gottlieb incorrectly diminishes the effectiveness of preventive measures. Numerous studies show that screening and cleaning can reduce MRSA infections in hospitals by as much as 90%, even in the absence of new drugs. Screening means identifying incoming patients carrying the germ, and then taking precautions to prevent it from spreading to other patients. Recent studies at Rush Medical College in Chicago and Boston University in Massachusetts show that training cleaners not to overlook surfaces and to allow detergents

to remain on surfaces for at least three minutes, rather than just giving a quick spray and wipe, can curb the spread of germs from patient to patient. Can hospitals afford screening and cleaning? They cannot afford not to do it. The evidence is compelling that these steps actually make

hospitals more profitable, and require almost no capital outlay. While waiting for the miracle cures, hospitals should implement MRSA screening and thorough cleaning. This two step strategy will save patients lives immediately, no matter how the bacteria morph. Betsy McCaughey, Ph.D. Chairman, Committee to Reduce Infection Deaths New York Dr. Gottlieb's op-ed carries an important message for all Americans. I agree with everything in his article, but he does not present the full extent of the problem nor does he address new and hopeful, innovative diagnostic and therapeutic developments. He discusses antibiotic resistance in well-published "superbugs" such as MRSA, but antibiotic resistance is also a growing threat in such common problems as urinary tract infection in nursing homes. Approximately 85 such infections per 100 long-term care beds occur each year. These

organisms show increasing resistance to even potent antibiotics. Dr. Gottlieb also does not mention the dangers of biofilm and nosacomial (hospital acquired) infections. Biofilm is a slime like matrix produced by micro-organisms as a defense mechanism against their environment. Biofilm is particularly dangerous to hospital patients whose first line defense against infection (their skin) has been breached by injury, surgery (particularly involving implants) and various types of catheters. This is the main cause of nosacomial infection, which involves two million patients and

90,000 deaths per year in the U.S. Antibiotics are ineffective in preventing and treating biofilm infections. The good news is that help may be on the way. A group that includes UCLA, the Veterans Administration of Greater Los Angeles and GeneFluidics Inc. of Santa Monica, Calif., and which is funded by the National Institutes of Health, published a promising new technique in the Journal of Clinical Microbiology last year. The diagnostic technique can rapidly (under 30 minutes) identify uropathogens in clinical urine by using an electrochemical DNA biosensor. The biosensor turns the genetic information of the bacteria into an electrical signal. This is analogous to a telephone, which turns voice into an electrical signal. Other new methods for rapidly testing antibiotic susceptibility are also currently being evaluated. Dr. Gottlieb outlines the limitations of current antibiotics and problems of bringing new antibiotics to the market. Antibiotics are substances produced or derived from one micro-organism which destroys or inhibits the growth of other micro-organisms. New antibiotics will be developed. However progress in antimicrobials will also be made. A new group of hopeful antimicrobial compounds called Aganocides (developed by Nova Bay Pharmaceuticals) are based on small molecules

generated by our own white cells that defend against invading pathogens. In the body these compounds are produced "on demand" and are transient. Important safety features include long shelf life, stability and very high therapeutic index (kills pathogens at concentrations significantly lower than concentration where it begins to harm human cells). Aganocides also unlikely to be rejected by the immune system and are unlikely to provoke bacterial resistance. They are also likely to kill bacteria in minutes, kill most, if not all species of bacteria, and kill certain viruses, yeast and fungi. And Aganocides may even kill resistant bacteria and destroy bacteria protected by biofilm. Current evidence indicates that a normal adult human has more bacteria in his body than his own DNA. In optimal condition, bacteria are divided every 20 to 30 minutes producing

billions of pathogens in a single day. These two facts alone guarantee that bacteria will always present problems for medical science. But new diagnostic and therapeutic developments will continue to allow us to be masters of our bodies.