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10 Oldest Known Diseases

HowStuffWorks “10 Oldest Known Diseases”.

In the study of ancient diseases, nothing speaks like the dead. “Bone abnormalities are a strong identification source,” said Dr. Anne Grauer, anthropologist at Loyola University Chicago and president of the Paleopathology Association, during a personal interview. So it’s relatively easy to date tuberculosis due to the lesions it leaves on bones. Pneumonia may be more ancient than TB, but lung tissue doesn’t hold up so well after being buried.

“Another source for dating diseases is genomic data,” said Dr. Charlotte Roberts, archaeologist at the University of Durham and author of the book “The Archaeology of Disease.” DNA testing of samples from mummies and skeletons can conclusively identify disease. And even without the evidence of a body, genes in existing samples of TB and leprosy bacteria suggest prehistoric origin.

But the most difficult trick in defining the oldest known diseases may be in how you define the word “disease.” For the purposes of this article, we’ll explore only human, infectious, viral or bacterial diseases. So nix tooth decay, psoriasis, gout, obesity, rickets, epilepsy, arthritis and other human difficulties that are perhaps best classified as “conditions.”

Notably absent from this list are some of history’s biggest killers, including influenza, measles, and the black plague. This is because these diseases require and the level of population density that didn’t develop until humans began living in cities. Influenza, measles, and the plague are social. Malaria isn’t.

We’ve listed 10 of the oldest known diseases, listed in no particular order. On the next page, we’ll get started with a condition that thrives in close quarters.

Around 400 B.C., the Athenian physician Hippocrates catalogued the diseases of his world. Cholera was on the list. But while Hippocrates provides the first proof of cholera beyond a reasonable doubt, the disease likely originated along the Ganges River while Athens was still a very young place.

Cholera lives in many of the world’s water sources, but it’s most dangerous when it has an environment in which there are many people among whom it can spread. The Ganges River happens to be one of the most ancient locations of human population density, and so it was long, long ago that upstream users gathered in the numbers needed to pollute the water for those downstream. In other words, as more people become infected with cholera, they pollute the water supply with more bacteria, which in turn infects more people.

Interestingly, the same problem might have been a major factor in the loss of troops in Hannibal’s march across the Alps. With a 50,000-soldier train, the troops and animals in front would have encountered pristine mountain streams, but those in back would have been forced to deal with putrid and potentially cholera-rich water [source: Hunt].

9: Typhoid

From 430 to 426 B.C., a great plague swept through the city-state of Athens. The historian Thucydides describes the symptoms:

“People in good health were all of a sudden attacked by violent heats in the head and the throat or tongue, becoming bloody and emitting an unnatural and fetid breath. When it fixed in the stomach, it upset it; and discharges of bile of every kind named by physicians ensued, accompanied by very great distress. If they passed this stage, and the disease descended further into the bowels, inducing a violent ulceration there accompanied by severe diarrhea, this brought on a weakness which was generally fatal.”

The disease couldn’t have come at a worse time. The plague contributed to Athens’ eventual loss to Sparta in the Peloponnesian War and a long hiatus for democracy in world history.

What was the cause of this plague?

8: Leprosy

The Bible passage Leviticus 13:2 reads, “When a man shall have in the skin of his flesh a rising, a scab, or bright spot, and it be in the skin of his flesh like the plague of leprosy; then he shall be brought unto Aaron the priest, or unto one of his sons the priests.”

But this isn’t the first concrete mention of the disease. That honor goes to the Egyptian “Ebers Papyrus,” written in 1550 B.C., which recommends, “If you examine a large tumor of Khonsu in any part of a man and it is terrible and it has made many swellings. Something has appeared in it like that in which there is air … Then you shall say concerning it: It is a swelling of Khonsu. You should not do anything against it” [source: Nunn].

While typhoid and cholera are fairly straightforward in their aggressive spread through water sources, leprosy relies on another dispersion strategy — that of dormancy. People can carry the bacteria that cause leprosy for 20 years or more before showing symptoms, and during this time can spread the disease.

One historical challenge in treating leprosy was diagnosis. In its early stages of expression, leprosy looks much like syphilis and somewhat like psoriasis. Misdiagnosis landed many psoriasis sufferers in leper colonies where many eventually did, ironically, contract and die from leprosy due to increased exposure.

7: Smallpox

Generally, the goal of mummification is to preserve soft tissue. So, as you would expect, Egypt provides a treasure trove of information on ancient, soft tissue diseases.

One of the first researchers to turn a paleopathological eye on Egyptian mummies was Sir Marc Armand Ruffer, who in his 1921 book “Studies of the Palaeopathology of Egypt” described three mummies with “dome shaped vesicles” extremely similar to those expected of smallpox [source: Ruffer]. The most ancient of these mummies was dated 1580 B.C. and the most recent was the mummy of Ramses V, who died in 1157 B.C. After his own inspection of the mummy, Donald R. Hopkins, who participated in the World Health Organization’s Smallpox Eradication Program, wrote of Ramses V, “Inspection of the mummy revealed a rash of elevated ‘pustules’, each about 2 to 4 millimeters in diameter, that was most distinct on the lower face, neck, and shoulders, but was also visible on the arms.” [source: Hopkins]

Is this conclusive? No, not necessarily, and to date there has been no modern analysis of Ramses V that could definitively determine if his condition was, in fact, smallpox. But the circumstantial evidence seems strong.

Smallpox is one of history’s greatest killers, responsible for 300 to 500 million deaths in the 20th century [source: Saint Louis University].

6: Rabies

Rabies is ingenious: Not only does it infect a host, but it also hijacks the host’s brain in a way that makes the host want to bite things. This is how rabies gets a ticket to ride. And it’s been doing it since at least 2300 B.C., when it was described in the Eshuma Code of Babylon [source: Rupprecht et al.]

The first person known to have survived rabies without a vaccination is Jeanna Giese, a Wisconsin teen who was bitten in 2004 by a rabid bat while at church. The New York Times reports that Jeanna went a month between bite and treatment, and was admitted to the hospital with symptoms of full-blown rabies [source: Rosenthal]. Doctors at the Children’s Hospital of Wisconsin initiated a cocktail of coma-inducing and antiviral drugs, though Giese’s family credits prayer with saving the girl’s life.

5: Malaria

The Romans offered the first cure for malaria: an amulet worn around the neck, inscribed with the powerful incantation “abracadabra” [source: Shah]. Over the years, we’ve attempted various other cures: adding oil to stagnant puddles to smother mosquito larvae, using pesticides, vaccines and nets, and even leveraging high-tech solutions such as a laser that shoots mosquitoes in midair. But the disease continues to infect 300 million people every year, killing 1 million of them [source: Shah].

The Wall Street Journal reports that malaria is responsible for half of all human deaths since the Stone Age [source: Shah].

Granted, that statistic extends the origin of the disease back in time past its first definite mention, which was in the Chinese “Nei Ching (“The Canon of Medicine”), around the year 2700 B.C. [source: CDC].

4: Pneumonia

People breathe more than 11,000 liters (3,000 gallons) of air every day [source: Nebraska Department of Environmental Quality]. And so, as you would expect, the lungs are a favorite home of bacteria, viruses, fungi and even parasites. And when anything foreign colonizes the lungs, the most common result is fluid. The umbrella term we use to describe fluid in the lungs is pneumonia.

Hippocrates wrote that fluid in the lungs should be called pneumonia if, “the fever be acute, and if there be pains on either side, or in both, and if expiration be if cough be present, and the sputa expectorated be of a blond or livid color” [source: Hippocrates]. But he also distinctly calls it a “disease of the ancients.”

Where exactly does pneumonia place in this list of oldest known diseases? Because it’s a soft tissue disease, the archaeological record isn’t strong. But it’s likely that various forms of pneumonia have been around as long as our lungs.

3: Tuberculosis

In 2008, a team of scientists from University College London excavated the submerged ancient city of Alit-Yam, off the coast of Israel. There, they found the buried remains of a mother and her child. Both skeletons showed bone lesions characteristic of tuberculosis [source: Lloyd]. DNA testing confirmed it: Tuberculosis is at least 9,000 years old.

Interestingly, this dig also lent evidence to an ongoing chicken-or-the-egg debate of whether we got TB from cows or they got it from us. In Alit-Yam, human skeletons showed signs of TB, while DNA from animal skeletons didn’t [source: Hershkovitz et al.]. So it seems cows are not the killers we once thought.

Other historical speculation has proved equally false: Neither the fossil nor DNA records support the cause of TB as nightly revelry with fairies and the resulting lack of rest, nor is the disease the result of witches who transform the victim into a horse and then ride the victim to nightly meetings, as were once thought [source: Briggs].

While the Alit-Yam finding is the oldest confirmed case of TB, characteristic lesions have been found on bones found in Turkey, dated about 500,000 years ago [source: Lloyd].

2: Trachoma

Trachoma is a chronic infection of the upper eyelid that eventually results in the eyelid constricting and turning the eyelashes in toward the cornea. Over time, the rubbing of the constricted eyelid and especially the eyelash makes the patient go blind. This is what happened to Aetius, Paulus Aeginetus, Alexander, Trailaus, Horace and Cicero. And trachoma is described in Hippocrates and in the Egyptian Ebers papyrus [sources: Siniscal and Nunn].

But researchers make a compelling case for earlier trachoma found in a corner of the world little associated with early diseases: Australia. Aboriginal skeletons from 8000 B.C. show a common skull lesion around the eyes [source: Webb]. Scientists determined that these lesions were due to bone infection that had come from soft tissue infection. Though there are a few eye diseases that could fit this bill, the skeletons were found in the Australian region in which trachoma is most common today.

1: Rocky Mountain Spotted Fever

Mitochondria are small organelles found in nearly every cell in the human body. And they perform a function essential to human life, converting glucose from food to energy called adenosine triphosphate, or ATP, which cells can use.

But Mitochondria carry their own genetic material — separate from human DNA — and these genes look a lot like those of bacteria. In other words, it’s very likely that the mitochondria that we depend on for survival are the products of an ancient infection [source: Andersson et al.].

Whatever the infection, it predates animal life, let alone humans. So there’s no use exploring the fossil record. Instead, researchers compared the genes of mitochondria to those of existing bacteria. The closest match was to bacteria of order Rickettsiales, many of which cause diseases — including Rocky Mountain spotted fever [source: Eremeeva and Dasch, Andersson et al.].

But remember, we’re talking about a disease that existed before animal life. So the oldest disease isn’t really Rocky Mountain Spotted Fever itself, but some unnamed proto-disease with genetic similarity.

Long, long ago bacteria invaded a cell. And because of this infection, we have life as we know it.

Read on to the next page for more infectious details.

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Malaria deaths fall 20% worldwide in last decade

BBC News – Malaria deaths fall over 20% worldwide in last decade.

There has been a fall of just over 20% in the number of deaths from malaria worldwide in the past decade, the World Health Organization says.

A new report said that one-third of the 108 countries where malaria was endemic were on course to eradicate the disease within 10 years.

Experts said if targets continued to be met, a further three million lives could be saved by 2015.

Malaria is one of the deadliest global diseases, particularly in Africa.

In 2009, 781,000 people died from malaria. The mosquito-borne disease is most prevalent in sub-Saharan Africa, where 85% of deaths occurred, most of them children under five.

An earlier report here incorrectly referred to a 40% drop in deaths.

It has been eradicated from three countries since 2007 – Morocco, Turkmenistan and Armenia.

The Roll Back Malaria Partnership aims to eliminate malaria in another eight to 10 countries by the end of 2015, including the entire WHO European Region.

Malaria Factfile

  • 2000: 233 million cases, 985,000 deaths
  • 2009: 225 million cases, 781,000 deaths
  • Malaria present in 108 countries and territories
  • 1.3% GDP reduction in heavily-infected countries

Robert Newman, director of the WHO’s Global Malaria Programme, said “remarkable progress” had been made.

“Better diagnostic testing and surveillance has provided a clearer picture of where we are on the ground – and has shown that there are countries eliminating malaria in all endemic regions of the world,” he told an international Malaria Forum conference in Seattle.

“We know that we can save lives with today’s tools.”

Global eradication

Graphic: Global Malaria deaths 2000-09

A global malaria eradication campaign, launched by WHO in 1955, succeeded in eliminating the disease in 16 countries and territories.

But after less than two decades, the WHO decided to concentrate instead on the less ambitious goal of malaria control.

However, another eight nations were declared malaria-free up until 1987, when certification was abandoned for 20 years.

In recent years, interest in malaria eradication as a long-term goal has re-emerged.

The WHO estimates that malaria causes significant economic losses, and can decrease gross domestic product (GDP) by as much as 1.3% in countries with high levels of transmission.

In the worst-affected countries, the disease accounts for: Up to 40% of public health expenditures; 30% to 50% of inpatient hospital admissions; and up to 60% of outpatient health clinic visits.

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Scientists reengineer antibiotic to overcome dangerous antibiotic-resistant bacteria

Scientists reengineer antibiotic to overcome dangerous antibiotic-resistant bacteria.

ScienceDaily (Aug. 25, 2011) — A team of scientists from The Scripps Research Institute has successfully reengineered an important antibiotic to kill the deadliest antibiotic-resistant bacteria. The compound could one day be used clinically to treat patients with life-threatening and highly resistant bacterial infections.

The results were published in an advanced online issue of the Journal of the American Chemical Society.

“[These results] have true clinical significance and chart a path forward for the development of next generation antibiotics for the treatment of the most serious resistant bacterial infections,” said Dale L. Boger, who is Richard and Alice Cramer Professor of Chemistry at The Scripps Research Institute and senior author of the new study. “The result could not be predicted. It really required the preparation of the molecule and the establishment of its properties.”

The compound synthesized is an analogue of the well-known commercial antibiotic vancomycin.

The new analogue was prepared in an elegant total synthesis, a momentous achievement from a synthetic chemistry point of view. “In addition to the elegantly designed synthesis,” said Jian Xie, postdoctoral fellow in Boger’s group and first author on the publication, “I am exceedingly gratified that our results could have the potential to be a great service to mankind.”

A Single Atom Changes Everything

Vancomycin is an antibiotic of last resort, which is used only after treatment with other antibiotics has failed. Clinically, it is used to treat patients that are either infected with the virulent methicillin-resistant Staphylococcus aureus (MRSA), individuals on dialysis, or those allergic to beta-lactam antibiotics (penicillin, cephalosporins).

The drug was first used clinically in the 1950s, and the first vancomycin-resistant bacterial strains were isolated in the 1980s.

Vancomycin normally works by grabbing hold of and sequestering the bacterial cell-wall making machinery, a peptidoglycan (carbohydrate and peptide containing molecule). Only Gram-positive bacteria have a cell wall, which is a membrane on the cell’s outer surface.

The antibiotic binds so tightly to the peptidoglycan that the bacteria can no longer use the machinery to make their cell wall and thus die.

Unfortunately, bacteria have found a way to alter the peptidoglycan in such a way that the antibiotic can no longer grab hold. Think of it as trying to hold a ball without any fingers. Biochemically the bacteria express a mutant form of the peptidoglycan in which properties of a key atom used in the recognition process are changed. This simply means where there once was something attractive there is now something repulsive. Chemically, the bacteria replace an amide (carbonyl, RC=O linked to an amine) with an ester (a carbonyl, RC=O linked to an oxygen, O).

This one atom change changes the entire game and renders vancomycin ineffective. Until now.

Reengineering Vancomycin

Like magnets, molecular interactions can be attractive (oppositely charged) or repulsive (identically charged). What chemists in the Boger lab have done is made this key interaction no longer repulsive, but attractive.

So now the new vancomycin analogue can grab hold of the mutant peptidoglycan, and again prevent the bacteria from making the cell wall and killing the resistant bacteria. But what is so remarkable about the design is that the redesigned antibiotic maintains its ability to bind the wild type peptidoglycan as well.

Changing the properties of a key amide at the core of the natural products structure required a new synthetic strategy that only the most talented chemists could achieve in the lab. The preparation of the entire structure took a great deal of time and a fresh approach.

The new compound has an amidine (an iminium, RC=NH+ linked to a nitrogen, N) instead of an amide at a key position buried in the interior of the natural product. However, to install such a functional group, the chemical properties of the amide carbonyl were not useful, as the natural product has seven of them.

Instead, the group relied on the chemical properties of sulfur (S), oxygen’s downstairs neighbor in the periodic table, to install the desired nitrogen. To do this, a second analogue was prepared in which the key amide was chemically altered to a thioamide. “The thioamide allowed us to make any modification at the residue 4 amide that we would like to make, such as the amidine, but we could also make the methylene analogue,” said Boger citing work published in another paper (B. Crowley and D. L. Boger, J. Am. Chem. Soc. 128: 2885-2892). “And there are other modifications that we are making at the present time that we haven’t disclosed. We are just getting to that work.”

The most fundamental finding in the synthesis was that the installation of the amidine could be done in the last step, as a single-step conversion, on the fully unprotected thioamide analogue. Providing an elegant and novel approach to the analogue, which contrasts other published multistep procedures. This chemical behavior was, as Boger said, “an astonishing result as there are no protecting groups and it is a single step reaction… in the end it was the simplest and most straightforward way to prepare the amidine.”

Although it is still at its early stages and there is much work ahead. Currently, the only route known to make the new antibiotic is the one published by Boger and his co-workers, which presently provides laboratory amounts of the compound. So Professor Boger now looks forward and will continue to investigate the “host of alternative approaches” for the preparation of the molecule “such as reengineered organisms to produce the material or semi-synthetic approaches to the analogue. That is going to be part of the next stage of the work.”

In addition to Boger and Xie, other contributors to the paper include Joshua G. Pierce, Robert C. James, and Akinori Okano.

The work was funded by the U.S. National Institute of Health (CA041101) and the Skaggs Institute for Chemical Biology.

Journal Reference:

  1. Jian Xie, Joshua G. Pierce, Robert C. James, Akinori Okano, Dale L. Boger. A Redesigned Vancomycin Engineered for Duald-Ala-d-Ala andd-Ala-d-Lac Binding Exhibits Potent Antimicrobial Activity Against Vancomycin-Resistant Bacteria. Journal of the American Chemical Society, 2011; 110816100911095 DOI: 10.1021/ja207142h

Crop disease to add to east Africa's woes

Crop disease to add to east Africa’s woes – environment – 13 July 2011 – New Scientist.

NEARLY 20 million people face starvation in east Africa as the region experiences its worst drought for 60 years. Hopes now focus on the return of the rains, perhaps as early as the autumn. But that could just bring another problem with it.

A new, aggressive strain of yellow rust, a fungal disease of wheat, is waiting in the wings, and east Africa isn’t the only region at risk.

The disease had already struck the US, Australia and Europe when, in 2010, a particularly virulent strain infested an area from Morocco to Pakistan, and spread faster than any known major crop disease (see map). Most wheat varieties in warm countries have no defence against it. Its march continued this year, with an outbreak in northern India.

Concern about yellow rust has languished as wheat scientists rushed to respond to a related disease, the Ug99 strain of stem rust against which little of the world’s wheat has any resistance. Yellow rust has historically been less deadly than stem rust, and thrived only in cool countries.

But in 2000, a new aggressive strain of the disease was detected in California, though it probably evolved in Africa or Asia, says Mogens Hovmøller of Aarhus University, Denmark. It generates more spores than its ancestors, so it spreads farther, faster.

It is also nastier. Yellow rust typically does not destroy entire crops, even in the absence of fungicide. But this lineage wiped out organic crops in Denmark, says Hovmøller. Based on the location of recent outbreaks, Colin Wellings of the University of Sydney in New South Wales, Australia, says some of the world’s major wheat producers are at risk from the new strain.

Concern is greatest in the tropics, where most farmers cannot afford fungicide and yellow rust has not typically been a problem: until now, the disease has not been adapted to warm temperatures. As a result, most local wheat varieties carry only one gene to resist it, called Yr27.

The new strain tolerates warmer temperatures and appears to have acquired genes to defeat Yr27, possibly from other yellow rusts. No one knows where or when this happened, but plant pathologists discovered last year that yellow rust can reproduce sexually, suggesting the new strain may have picked up genes from local strains by mating with them.

The result was an epidemic that in 2010 killed up to 40 per cent the wheat crop in Ethiopia, Syria, Turkey, Iran, Azerbaijan, Iraq, Uzbekistan, Morocco and Kenya. The spores like humidity, and struck irrigated fields in drought-stricken areas, says Mahmoud Solh, head of the International Center for Agricultural Research in the Dry Areas (ICARDA) in Aleppo, Syria. Drought is now holding them at bay in some places, but “when the rains return to Africa, the rust will be waiting”, he warns. Hovmøller agrees.

Wheat researchers meeting at ICARDA in April said they had developed wheat varieties that can resist the new strain of yellow rust. They also yield 15 per cent more grain and resist Ug99 stem rust. But it will take several years to breed enough seed for regions blighted by the new strain, cautions Solh. And the aggressive strains produce so many spores so fast, adds Hovmøller, that they mutate and adapt faster than yellow rust has in the past. “What works now may not last long,” he says.

Scientists discover first gonorrhea strain resistant to all available antibiotics

Scientists discover first gonorrhea strain resistant to all available antibiotics.

 

ScienceDaily (July 11, 2011) — An international research team has discovered a strain of gonorrhea resistant to all currently available antibiotics. This new strain is likely to transform a common and once easily treatable infection into a global threat to public health.

The details of the discovery made by Dr. Magnus Unemo, Dr. Makoto Ohnishi, and colleagues will be presented at the 19th conference of the International Society for Sexually Transmitted Disease Research (ISSTDR) which runs July 10-13 in Quebec City, Canada.

The team of researchers successfully identified a heretofore unknown variant of the bacterium that causes gonorrhea, Neisseria gonorrhoeae. Analyzing this new strain, dubbed H041, allowed researchers to identify the genetic mutations responsible for the bacterium’s extreme resistance to all cephalosporin-class antibiotics — the last remaining drugs still effective in treating gonorrhea.

“This is both an alarming and a predictable discovery,” noted Dr. Unemo of the Swedish Reference Laboratory for Pathogenic Neisseria. “Since antibiotics became the standard treatment for gonorrhea in the 1940s, this bacterium has shown a remarkable capacity to develop resistance mechanisms to all drugs introduced to control it.”

“While it is still too early to assess if this new strain has become widespread, the history of newly emergent resistance in the bacterium suggests that it may spread rapidly unless new drugs and effective treatment programs are developed,” Dr. Unemo continued.

Gonorrhea is one of the most common sexually transmitted diseases in the world. In the U.S. alone, according to the Center for Disease Control and Prevention (CDC), the number of cases is estimated at 700,000 annually.

Gonorrhea is asymptomatic in about 50% of infected women and approximately 2-5% of men. When symptomatic, it is characterized by a burning sensation when urinating and pus discharge from the genitals. If left untreated, gonorrhea can lead to serious and irreversible health complications in both women and men.

In women, the infection can cause chronic pelvic pain and ectopic pregnancy. It can lead to infertility, mostly in women but also in men, and it increases the risk of HIV transmission. In 3-4% of cases, untreated infections spread to the skin, blood, joints, or even the heart and can cause potentially mortal lesions. Babies born of infected mothers are at high risk of developing serious blood and joint infections, and passage through the birth canal of an infected mother can cause blindness in the infant.

from materials provided by Université Laval, via EurekAlert!, a service of AAAS.

 

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Acceptance, not access, the biggest hurdle to eradicating disease

Shot in the Dark – By Charles Kenny | Foreign Policy.

In 2009, veterinarians at the U.N. Food and Agriculture Organization made a remarkable announcement: Rinderpest, a livestock-borne disease, would soon be eradicated. OK, so maybe it wasn’t front-page news, but rinderpest — which causes animals to develop fever, followed by diarrhea and (frequently) death — has over thousands of years been a recurring plague on human civilization. It has destroyed the food supplies of entire countries such as Ethiopia, which lost a third of its population to a rinderpest-related famine in the late 19th century. The FAO’s eradication effort, launched in 1992, marks only the second time a disease has been deliberately wiped off the face of the Eearth; the first, better-known case was smallpox, which killed between 300 million and 500 million people over the course of the 20th century before its eradication in 1980.

On June 13, the global community tried for a repeat performance with a pledge drive, held by the Global Alliance for Vaccines and Immunization (GAVI). Thanks to support from aid agencies from Britain to Russia, as well as the Gates Foundation, GAVI raised $4.3 billion to immunize 250 million kids worldwide between now and 2015, protecting against diseases from tetanus to tuberculosis, whooping cough to diphtheria. It’s a daunting project, but one that is less implausible than it once was: The range of diseases that can be prevented is growing ever longer, and now includes HPV, rubella, typhoid, and Japanese encephalitis. Vaccines for malaria and dengue fever may not be far behind, and there’s even some hope for HIV. GAVI itself boasts a strong track record: Over the organization’s first decade, more than 5 million child deaths were prevented though more rapid introduction and increased coverage of vaccines in low-income countries. But, going forward, the alliance is going to have to think more about getting parents to vaccinate their kids — the demand side of health– especially if it wants to repeat the huge victory of wiping out a disease.

 

Although few in the public-health NGO community would like to admit it, eradicating diseases is at least as dependent on luck as it is on planning and persistence. Universal vaccination — the only nearly surefire means of eradication — is an impossibility in most countries. Even the best-resourced campaigns have to deal with the trouble of reaching remote villages over rutted roads to deliver vaccines that sometimes need to be kept refrigerated, often are difficult to administer, and can take multiple shots to take effect. Add to that the challenge of reaching people who often have no official registration or address, and you can see the problem.

Health professionals instead rely on the strategy of trying to vaccinate enough people, especially in the immediate period of an outbreak, so that the disease eventually retreats toward extinction — always a dicey prospect. Donald Henderson at Johns Hopkins University wrote of smallpox eradication that it “was achieved by only the narrowest of margins” while progress “wavered between success and disaster, often only to be decided by quixotic circumstance or extraordinary performances by field staff.”

Today, the world appears to be walking the same knife-edge with polio. The Global Polio Eradication Initiative was launched in 1988 when there were about a third of a million cases worldwide. Indigenous polio was eradicated in the Americas in 1991 and China in 1996. By 1997, the worldwide total of cases was down to 7,000; by 2009, there were only 1,600. But new cases keep popping up: That same year saw outbreaks in Uganda, Mali, Togo, Ghana, Ivory Coast, and Kenya.

The problem wasn’t vaccine supply; the world has spent $8.2 billion on eradication programs, which bought both vaccines and the human infrastructure required to deliver them. Rather, it was a demand issue, one that hinged in particular on the attitude of governments and parents.

Take the example of the polio vaccination campaign in northern Nigeria in 2003, which responded to a particularly virulent outbreak that was threatening to spread. The governor of Kano state refused to support the vaccination campaign because of rumors that the vaccines were laced with drugs that would sterilize recipients — which he claimed was part of a U.S. conspiracy to depopulate the developing world.

To be fair to Kano’s former governor, only 23 percent of children across the whole of Nigeria were fully immunized in 2008, suggesting that general lack of information, fear of side effects, and the hassle of getting kids vaccinated probably played the larger part in low takeup of polio vaccine on the demand side (not to mention weaknesses in the vaccine delivery and administration system). But that only emphasizes the fact that without at least some support from both local officials and parents, there is no way to complete a vaccination program.

Issues with government prioritization help to account for the fact that about 55 percent of surveyed kids are fully vaccinated in low-income countries, according to my colleague Amanda Glassman at the Center for Global Development — but only 42 percent in lower-middle-income countries are. And in fact, demand-side problems affect the whole world, not just the developing parts of it that are typically the focus of immunization efforts. More and more parents in Europe and the United States have refused to vaccinate their kids over the fear (despite overwhelming evidence to the contrary) that the vaccines lead to autism.

What about the less conspiracy-minded corners of the world? MIT economists Abhijit Banerjee and Esther Duflo, authors of this year’s development blockbuster Poor Economics, studied vaccination rates in Udaipur, India and found that only 16 percent of children below age 2 there were fully immunized against the standard preventable diseases. That was due in part to the limited provision of immunization clinics, but it was also because of low demand for the free immunizations that were available: Even when a local NGO helped ensure regular and well-publicized visits by traveling immunization camps in parts of Udaipur, full immunization only increased from 6 percent in control villages to 18 percent in villages that saw regular camps. World Bank research in India suggests one reason why — many parents do not fully appreciate the health benefits of vaccination and so are unwilling to go to the effort of attending an immunization camp.

One effective response if the kids won’t come to the vaccines is to take the vaccines to the kids. If families are visited at home by a trusted health worker, the World Bank research suggests parents are very happy to see their kids stuck full of needles. But the trouble with such an approach is that house visits are a very expensive way to guarantee coverage. So Banerjee and Duflo tried adding an incentive to get parents to bring their kids to camps, instead — a 2-pound bag of lentils for each immunization and a set of plates if parents ensured their kids got the full program. That more than doubled the full immunization rate to 39 percent in villages where the incentives were offered and even increased immunization rates threefold in neighboring villages. And because the incentives increased the efficiency of the camps (i.e., how many kids were vaccinated each day), they actually reduced the overall cost of providing immunization coverage, from $56 per child without incentives to $28 per child.

The long-term answer to raising vaccination levels worldwide is to spread knowledge of their safety and efficacy. But as both the polio vaccine scare in Nigeria and the recent gross irresponsibility of a doctor and his Hollywood acolyte over vaccines in the West demonstrate, that process can be complex. In the meantime, providing direct incentives to people to get their kids vaccinated are likely to have a more immediate impact on changing behavior — and that will reduce both the immense human costs of infectious disease and the considerable financial costs of preventing them.

Charles Kenny is a senior fellow at the Center for Global Development, a Schwartz fellow at the New America Foundation, and author, most recently, of Getting Better: Why Global Development Is Succeeding and How We Can Improve the World Even More. “The Optimist,” his column for ForeignPolicy.com, runs weekly.

CDC Calls for New Biosurveillance to Halt Disease Spread

CDC Calls for New Biosurveillance to Halt Disease Spread: Scientific American.

By Gayathri Vaidyanathan of Nature magazine

Germany is still recovering from one of the world’s worst outbreaks of enterohaemorrhagic Escherichia coli, which as of 18 June had sickened more than 3,200 people and caused 39 deaths. The unusually deadly bacteria moved undetected through the food supply from livestock to agriculture to the dinner table, and the response to the outbreak was branded slow and inefficient by physicians and scientists (see ‘Microbe outbreak panics Europe‘).

Now a group of health professionals assembled by the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, has called for biosurveillance efforts in the United States and worldwide to be streamlined to help recognize and respond to threats quickly.

“We are trying to create an international immune system, a system that has the capacity to recognize abnormalities,” says Ian Lipkin, co-chair of the National Biosurveillance Advisory Subcommittee (NBAS) and director of the Center for Infection and Immunity at the Mailman School of Public Health at Columbia University, New York.

The NBAS report, Improving the Nation’s Ability to Detect and Respond to 21st Century Urgent Health Threats, is the second by the group originally assembled by former President George W. Bush over fears about bioterrorism. The report is now under consideration by the White House and the US Department of Health and Human Services.

Unified approach

The report recommends that the various US federal agencies that monitor infectious disease combine their operations. Currently, disease outbreaks are monitored by the CDC, the US Department of Agriculture, the Food and Drug Administration, the defense department, the Department of Homeland Security and state-level health agencies. The NBAS report calls for more common language and more ‘data liquidity’ between the agencies to promote the sharing of information. This would also allow better analyses to help detect relevant patterns in health complaints.

The NBAS wants the hub of biosurveillance to move from the CDC to the White House. This would free up agency budgets to invest in a program currently lacking in the United States and globally: surveillance of domestic animal, wildlife, plant, food, vector, disease and environmental sources, integrated with monitoring of human health.

“It is clear given the events of the recent past, like the E. coli outbreak, that we weren’t prepared to deal with it,” says Lipkin. “We don’t have common terminology, we don’t have boots on the ground, we don’t have people who have the capacity to recognize these risks, analyze them and present them in a way policy-makers can appreciate.”

Disparate data

It took weeks before bean sprouts were finally identified as the source of the German E. coli outbreak, and a second, isolated outbreak in France has shifted suspicion to sprouted seeds. Yet the German outbreak is instructive, according to David Fisman, an epidemiologist at the Dalla Lana School of Public Health at the University of Toronto, Canada. If there had been a centralized database tracking pathogen profiles in animals, food and the environment–information that already exists at some level within disparate agricultural, food and drug, and human health agencies–it wouldn’t have taken so long to isolate the cause of the outbreak, says Fisman.

A good tracking system would include pathogen profiles in a global database, according to Jorgen Schlundt, director of food safety, zoonoses and foodborne diseases at the World Health Organization headquartered in Geneva, Switzerland. In the event of disease, physicians would do a database search to discover where else the pathogen is found in the environment to try to stop infections at the source.

“The way we’ve done it in the past, you wait until you find them [the pathogens] in the humans and then you go back and say ‘okay, where did that come from?’,” he says. “But if everything was working in a good way, you would find them in the animal production units and then you’d prevent them getting to humans.”

Funding for the proposals in the NBAS report would have to be figured out in this era of budget cuts and austerity, but Lipkin is optimistic. “There’s going to be concern about investing here, but we think that if you take a look at the investments being made by all these agencies and you consider what would happen if we had an organized approach to this, I’m not even certain it would cost more money.”

This article is reproduced with permission from the magazine Nature. The article was first published on June 28, 2011.

Is Drug Resistance in Humans Coming From Chickens?

Is Drug Resistance in Humans Coming From Chickens? | Wired Science | Wired.com.

There’s a new paper out in the CDC’s journal Emerging Infectious Diseases that makes a provocative claim: There is enough similarity between drug-resistance genes in  E. coli carried by chickens and  E. coli infecting humans that the chickens may be the source of it.

If it is correct — and it seems plausible and is backed by past research — the claim provides another piece of evidence that antibiotic use in agriculture has a direct effect on human health.

Here are the details:

The paper is a collaboration by researchers from several hospitals in the Netherlands, plus the Netherlands’ National Institute of Public Health and Environmental Protection, the University of Birmingham and a section of the UK’s National Health Service. They isolated E. coli from patients in four Dutch hospitals over 2.5 months in 2009, and compared those with E. coli strains isolated from randomly chosen supermarket meat that was bought in the hospitals’ local areas during the same time period. They compared both those sets of isolates against a third set, of E. coli from blood cultures taken from patients in the hospitals during the same months.

In each set of samples, they were looking at the E. coli to see whether they harbored genes for the type of resistance known as ESBL, for “extended-spectrum beta-lactamase,” an enzyme that denatures a category of drugs used for serious infections that occur mostly in hospitals. When the extended-spectrum beta-lactams no longer work, only a few last-resort drugs are left. (Back in the 1980s, the most common genes for ESBL were blaTEM or blaSHV, but in the past 10 or so years there has been a rapid global increase in the occurrence of a different ESBL gene, blaCTX-M.)

Here’s what they found:

  • Out of 876 patients tested by rectal swab — because E. coli is a gut bacterium, carried in and spread by feces — 45 (5 percent) harbored ESBL genes.
  • Out of 31 blood cultures in the hospitals’ labs, 23 (74 percent) contained ESBL genes.
  • Out of 262 meat samples, 79 (30 percent) harbored an ESBL gene. Broken down by type of meat, there was ESBL in 80 percent of the chicken samples, 5 percent of the beef, 2 percent of the pork, and 9 percent of ground or otherwise mixed meat.

When they broke down the organisms by type, they looked like this. Note the amount in each pie chart that is given over to the ESBL genes blaCTX-M, and the significant correspondence of blaCTX-M-1 in red.

When they put the genes through a second level of genetic analysis, multi-locus sequence typing, 57 percent of the rectal specimens and 57 percent of the blood cultures were closely related to the strains in the chicken meat.

There’s an important backdrop to this research. The Netherlands has one of the lowest rates of human antibiotic resistance in the world, thanks to especially stringent infection control and drug-conservation policies. Paradoxically, it has the highest rate of antibiotic use in agriculture in Europe. As a result, when something starts to move into humans, it is easier to distinguish, because there is no “background noise” of high rates of hospital and community drug resistance such as there are in the US. And because there are no competing resistance factors from other sources, it is easier to identify and explain.

Thus, the researchers can comfortably say:

We conclude that the high rate of ESBL contamination of retail chicken meat in the Netherlands, which involves many of the same ESBL genes present in colonized and infected humans, is a plausible source of the recent increase of ESBL genes in the Netherlands. The similarity of E. coli strains and predominant drug resistance genes in meat and humans provides circumstantial evidence for an animal reservoir for a substantial part of ESBL genes found in humans.

If something about this research sounds familiar, it’s because a similar study was published a few months ago, also from the Netherlands, with a partially overlapping analysis: chicken meat and blood-culture records, but no swabs from simultaneous patients. That study too found a high degree of correlation between ESBL-containing organisms in humans and in chickens.

These findings won’t come as a surprise to anyone who accepts — as most good science and a number of public health authorities do — that antibiotic overuse in large-scale farming creates drug-resistant organisms that affect human health. The question, for those who don’t accept such a link, is: How much evidence is enough?

(Footnote: In addition to being published in EID, this study was also presented by Dr. Jan Kluytmans, the senior author, during the World HAI Forum taking place this week in France. I’ll have more on the HAI Forum in a future post.)

Cite: Overdevest I et al. Extended-spectrum ?-lactamase genes of Escherichia coli in chicken meat and humans, the Netherlands. Emerg Infect Dis. 2011 Jul. http://www.cdc.gov/EID/content/17/7/1216.htm