The Birth of Ebola

May 11, 2015 by

May 1, 2015

By Medical Discovery News

Colorized micrograph of Ebola by Dr. F.A. Murphy

For most Americans, the Ebola scare seems to have come and gone, but that doesn’t mean the outbreak is over in Africa or that we’ve seen the last of the virus, especially considering its history. Scientists believed that Ebola is relatively new as far as viruses go – only 10,000 years old. However, ancient animal bones show that Ebola appeared between 16 and 23 million years ago, perhaps even earlier.

The Ebola virus was discovered in 1976 during two outbreaks in what was then called Northern Zaire (now the Democratic Republic of the Congo) and Southern Sudan. The outbreaks were actually caused by two different strains of the Ebola virus named Zaire and Sudan, with 90 and 50 percent mortality rates respectively. Since then, three other strains have been identified: Tai Forest, Bundibugyo, and Reston, which is the only one that doesn’t affect people. Overall, there have been 27 outbreaks, but the current outbreak that started in March 2014 is by far the worst, infecting almost 25,000 people and killing over 10,000, thereby making it the world’s first Ebola epidemic.

Ebola is a member of the filovirus family, which also includes the Marburg virus discovered in 1967. Filoviruses are zoonotic, meaning they replicate in other animals, their natural reservoirs, before transmitting to humans. The Ebola virus’s natural reservoir is African fruit bats, so it can transfer to humans who come into contact with an infected bat or another species that has been infected, such as chimpanzees, antelope, and porcupine. Then the virus can spread from person to person.

New research into the origins of filoviruses shows that they have evolutionary ties that go back millions of years. Scientists tracked the viruses’ origins by looking for pieces of their genetic information in fossilized animal bones. While using the bones to study the genomes of ancient voles and hamsters, they found the same pieces of the viruses’ genetic material in the same locations in both rodent species. This suggests that the viruses have existed at least as long as the two species have.

Given the billions of bases each animal has in its genome, it is highly unlikely that these fragments of viral genetic information would have been inserted in exactly the same locations during different infections. Scientists therefore concluded that the virus had infected a common ancestor of these two rodents sometime before the Miocene Epoch, 5-23 million years ago, around the time the great apes arose. Furthermore, the viral genetic elements more closely resemble Ebola than Marburg, meaning the two viruses had already diverged from each other. Sometime before then, the two viruses shared a common ancestor that has not yet been identified.

This means that these viruses have been coevolving with mammals for millions and millions of years, much longer than previously believed. An understanding of the origins and evolution of filoviruses could help us better prevent outbreaks of them and hopefully even create a vaccine that would be effective against all of them.

For a link to this story, click here.

Filed Under: Health Tagged With: , , , , , , , , , , , , , , , , , , , , , ,

The Bright Side of Black Death

April 25, 2015 by

April 17, 2015

By Medical Discovery News

Bright Side of Black Death

It’s easy to think that nothing good could come from a disease that killed millions of people. But Dr. Pat Shipman, an anthropologist at Pennsylvania State University, disputed that notion in his recent article in “American Scientist,” where he suggested the Black Death that ravaged Europe in the Middle Ages may have resulted in some positive effects on the human population. Considering that we are in the midst another significant plague (the Ebola virus in West Africa), we could certainly use more information about the role of pandemics on human populations.

The Black Death or Bubonic plague started in the mid-1300s and was caused by a bacterium called Yersinia pestis, which typically enters the body through the bite of a flea. Once inside, the bacterium concentrates in our lymph glands, which swell as the bacteria grow and overwhelm the immune system, and the swollen glands, called buboes, turn black. The bacteria can make their way to the lungs and are then expelled by coughing, which infects others who breathe in the bacteria. The rapid spread of the infection and high mortality rates wiped out whole villages, causing not only death from disease but starvation as crops were not planted or harvested. It killed somewhere between 100 million to 200 million people in Europe alone, which was one-third to one-half of the entire continent’s population at the time. The plague originated in the Far East and spread due to improved trade routes between these two parts of the world.

Today, global travel is easier than ever thanks to extensive international airline networks. Just like with the Black Death, our transportation systems could enhance the spread of a modern plague. Of course, modern healthcare is also more sophisticated and effective, but as the latest Ebola outbreak has reminded us, a pandemic is a realistic possibility.

Dr. Sharon DeWitte, a biological anthropologist at the University of South Carolina, recently made several discoveries from comparing the skeletal remains of those who died from the Black Death and those who died from other causes during the same era. First, she found that older people, who were therefore already frail, died at higher rates. Killing this group at a higher rate created a strong source of natural selection, removing the weakest part of the population.

After the plague years, she found that in general people lived longer. In medieval times, living to 50 was considered old age. But the children and grandchildren of plague survivors lived longer, probably because their predecessors lived long enough to pass on advantageous genes. Today, a genetic variant in European people called the CCR5-D32 allele, which was favored during the natural selection initiated by the plague, is associated with a higher resistance to HIV/AIDS.

Microbes have an intimate relationship with human populations and have shaped human evolution through the ages. We may see survivors of the Ebola virus passing on similarly advantageous genes through natural selection as well.

For a link to this story, click here.

Filed Under: Uncategorized Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , ,

Quick Diagnosis for Early Treatment

December 19, 2014 by

Dec. 12, 2014

By Medical Discovery News

Quick Diagnosis for Early Treatment

The time it takes to test for the cause of an infection ranges from minutes to weeks. A new generation of biosensors may change that, as they are being developed to identify the viral, bacterial, or fungal origin of an illness within a few hours, allowing physicians to begin the correct treatment sooner.

Many infections have symptoms that resemble the flu, such as HIV, the fungal infection coccidioidomycosis, Ebola, and even anthrax. This makes it very difficult to make a diagnosis. The emergence of new microbial pathogens such as SARS and MERS and bacterial resistance to antibiotics only adds to the fight against infectious agents. Scientists like Louis Pasteur and Robert Koch developed the traditional method for diagnosing infectious disease about 150 years ago, and modern methods have improved their discoveries.

Viruses, bacteria, and fungi have genetic information contained in DNA, RNA, or both. Each strand of DNA or RNA is made of four kinds of building blocks called nucleotides: adenine (A), cytosine (C), guanine (G), and thymine (T) in DNA or uracil (U) in RNA. Every species has a unique genetic code as seen in its arrangement of nucleotides, and by unlocking that code scientists can determine their identity. Each of the nucleotides has a different molecular weight, so the number of each nucleotide in a strand of DNA or RNA can be determined by measuring it on a device called a mass spectrometer. This can identify a microbial pathogen faster than the traditional culturing method, and can also identify those that can’t be grown in a lab.

However, the massive amount of DNA and RNA in a patient’s own cells complicates things. To tackle this problem, inventors of the new biosensor have coupled a mass spectrometer with polymerase chain reaction (PCR) to amplify any piece of genetic information that matches a known sequence from a pathogen. The sensor can then detect a very broad array of potential pathogens simultaneously.

Scientists have been very careful in selecting the unique genetic regions of various pathogens for this test. Once the PCR is used to amplify pieces of potential pathogens in the sample, the mass spectrometer spits out a series of numbers that can be cross-referenced to a database of over 1,000 pathogens that cause human disease in just a few hours.

For example, two children were hospitalized with flu-like symptoms in Southern California in 2009. They tested positive for the flu virus, but doctors did not know which strain of the flu they had. The new sensor analyzed their samples and revealed that both children were infected with H1N1, otherwise known as swine flu, which was not circulating at that time. H1N1 became a pandemic strain with cases all around the world.

This new technology represents a universal pathogen detector, capable of identifying the organism responsible for a person’s illness in just a few hours. Networking the detectors between hospitals and health departments would quickly identify outbreaks and possibly save lives.

For a link to this story, click here.

Filed Under: Health Tagged With: , , , , , , , , , , , , , , , , , , , , , ,

Semi-Precious Pathogens

October 17, 2014 by

Oct. 17, 2014

By Medical Discovery News

Bug in amber

Some diseases are older than others. AIDS, for instance, is a recent phenomenon, while malaria has plagued humans for millennia. Recently, scientists examining ticks fossilized in amber found they were infected with bacteria similar to those that cause Lyme disease, a spirochete named Borrelia burgdorferi. Lyme disease is a bacterial infection caused by the bite of an infected tick. The discovery of an ancient Borrelia-like bacterium, now named Palaeoborrelia dominicana, shows that tick-borne diseases have been around for millions of years.

Lyme disease was identified in the early 1970s when mysterious cases of rheumatoid arthritis struck children in Lyme, Conn., and two other nearby towns. The first symptom is a rash called erythema migrans, which begins with a small red spot where the tick bite occurred. Over the next few days or weeks, the rash gets larger, forming a circular or oval red rash much like a bull’s eye. This rash can stay small or can cover the entire back. But not everyone with Lyme disease gets this rash, and the other symptoms, including fever, headaches, stiff neck, body aches, and fatigue, are common to many other ailments. Some people develop symptoms of arthritis, nervous system problems, or even cardiac issues.

Lyme disease can be difficult to diagnose. Sometimes, people write off their initial symptoms as the flu or another common illness, and experience symptoms for months or even years before finding the true cause. To diagnose Lyme disease, doctors measure the levels of antibodies the body produces in response to Borrelia infection. Lyme patients are treated with antibiotics, but if the bacteria have been in the body for a long period of time, it can take a long time to cure. The sooner diagnosis and treatment begin, the more quickly and completely patients will recover. Even after treatment for Lyme disease, people can still experience muscle or joint aches and nervous system symptoms.

Scientists from Oregon State University have studied 15- to 20-million-year-old amber found in the Dominican Republic. Despite existing for millions of years, bacteria are rarely found in fossils. However, free-flowing tree resin traps and preserves material such as seeds, leaves, feathers, and insects in great detail. Amber is then formed from the fossilization of the resin over millions of years as it turns into a semi-precious stone. This is the oldest fossil evidence of ticks containing such bacteria.

Four ticks from the Dominican amber were examined and found to have large populations of spirochetes that resemble the Borrelia bacteria, such as those that cause Lyme disease today. The oldest reported case of Lyme disease was Oetzi, a well-preserved natural mummy who lived 5,000 years ago and was discovered by hikers in the Alps. In other studies, fossils have revealed bacteria such as Rickettsia, which cause modern diseases like Spotted Fevers and Typhus, found in ticks from about 100 million years ago. Evidence suggests that even dinosaurs may have been infected with Rickettsia, showing these microbes likely infected other creatures before humans were added to the mix. Millions of years of co-evolution resulted in highly adapted pathogens that scientists and physicians still struggle to understand and treat.

For a link to this story, click here.

Filed Under: Health Tagged With: , , , , , , , , , , , , , , , , , , , , , ,

Hope for Sickle Cell

September 20, 2014 by

Sept. 19, 2014

By Medical Discovery News

While sickle cell disease has long been studied, a recent discovery revealed that the disease significantly increases the levels of a molecule called sphingosine-1-phosphate (S1P), which is generated by an enzyme called sphingosine kinase 1 (SphK1). Inhibiting the enzyme SphK1 was found to reduce the severity of sickle cell disease in mice, which will hopefully lead to new drugs that target SphK1in order to treat sickle cell disease in humans.

Sickle cell disease is caused by a change in the gene that is responsible for a type of hemoglobin, the protein molecule in red blood cells that carries oxygen. This tiny change results in hemoglobin clumping together, changing the shape of red blood cells.

The name for sickle cell disease actually comes from misshapen red blood cells. Rather than being shaped like a disk, or a donut without a whole, sickle cells are shaped like a crescent, sort of bending over on themselves. The normal shape is critical to red blood cells’ ability to easily travel through blood vessels and deliver oxygen to cells and tissues. Sickle cells become inflexible and stick to each other, blocking the flow of blood through blood vessels.

Symptoms of the disease begin to appear at about four months of age. Normally, red blood cells live for about 120 days. Sickle cells only survive 10-20 days. Although the bone marrow tries to compensate for the rapid loss of red blood cells, it cannot keep up. The disease causes pain, anemia, organ damage, and possibly infections.

Although the symptoms and their severity vary, most people with sickle cell disease will have periodic crises lasting hours or days. Symptoms include fatigue, paleness, shortness of breath, increased heart rate, jaundice, and pain. Long-term damage can occur in the spleen, eyes, and other organs, and sickle cell disease increases the risk of stroke. People who only inherit one copy of the sickle cell hemoglobin gene have a milder case of the disease than those who inherit two copies, one from each parent.

Current treatments only reduce the number and the severity of crises using hydroxyrurea, blood transfusions, pain medications, and antibiotics. As the disease advances, dialysis, kidney transplants, eye surgeries, gall bladder removal, and other treatments may be necessary. The only cure for the disease is a bone marrow transplant, which is not an option for everyone.

So it’s pretty exciting that when scientists found that levels of S1P were elevated in mice with sickle cell disease, they inhibited the enzyme SphK1 to reduce the levels of S1P. As a result, red blood cells lived longer and had less sickling. The mice also had less inflammation and tissue damage, which would reduce damage to red blood cells and prevent symptoms of the disease. When they engineered sickle cell disease mice without the gene for the enzyme SphK1 that makes S1P, again the mice had less sickling and symptoms.

How does S1P influence sickling? Apparently, it binds directly to hemoglobin and reduces its ability to collect and carry oxygen, which causes the characteristic folding of cells. S1P has other roles in the body, so it is unknown whether inhibitors to SphK1 can safely and effectively be used in humans to treat sickle cell disease.

For a link to this story, click here.

Filed Under: Health Tagged With: , , , , , , , , , , , , , , , , , , , ,

Death Not By Assassination

April 26, 2013 by

April 26, 2013

By Medical Discovery News

On July 2, 1881, President James Garfield walked into the waiting room of the Baltimore & Potomac Railroad terminal in Washington, D.C., with his two sons, ready to start his summer vacation in New England. But he had no idea what, or rather who, had been waiting for him. Suddenly, shots were fired at point-blank range behind the president, hitting him in the back. The assassin, Charles J. Guiteau, was an escaped mental patient suffering from delusions.

After superficial examination, physicians agreed that a bullet had hit the liver and lodged in the front wall of the abdomen. They decided that the wound was not necessarily fatal and the President was moved back to the White House.

Surviving a bullet wound depends upon the path of the bullet and where it ended up. If it was lodged in an organ, removing it through surgery was the only option. Otherwise, surgery was delayed until the patient was more stable, or the bullet was simply left in the body. Since X-rays had not yet been invented, physicians would manually probe for a bullet with unwashed fingers and unsanitary instruments, raising the risk of infection.

The physician Willard Bliss took control of President Garfield’s care. Bliss delayed the surgery to remove the bullet. Several times a day, he probed the wound in attempts to locate it. Even though English surgeon Joseph Lister had been promoting hand washing and the use of sterile instruments, many physicians including Bliss resisted this “as too much trouble.”

Newspapers, physicians, and citizens across the country weighed in on how to best treat the President. Even Alexander Graham Bell, who had recently invented the telephone, stepped in. He collaborated with Simon Newcomb to develop a device that could detect metal objects in the body. They tested their device by hiding bullets in bags of grain, sides of beef, and on themselves. As a final test, they took their device to the Old Soldiers Home in Washington, D.C., and successfully detected bullets inside Civil War veterans.

On July 26, they went to the White House to try to locate Garfield’s bullet. Bliss insisted that Bell only look for the bullet on the wrong side of Garfield’s body. But the metal detector went off everywhere they tested on him. What Bell did not know was that Garfield was lying on a new type of bed with coiled metal springs.

With Bliss continuing to probe for the bullet still inside, the President developed a fever and other signs of infection. He lingered in agony until his death from a massive infection on September 19, 1881. An autopsy revealed that the bullet had missed his spinal cord and all vital organs and come to rest in the fat tissue of his back, which was not a fatal blow.

President Garfield’s story ends with Vice President Chester Alan Arthur sworn in on the night of his death and the execution of Guiteau on June 30, 1882. However, it was not Guiteau’s bullet that killed the President, but the physician’s incompetent attempts to care for him.

For a link to this story, click here.

Filed Under: Uncategorized Tagged With: , , , , ,