Just when you thought it was safe to swim in the Atlantic off Florida comes a report of a very virulent strain of MRSA (a flesh eating virus) which has affected at least one swimmer and several fishing boat crew: www.floridatoday.com/topstories/102103bacteria.htm
For those of you who haven't seen MRSA at work imagine if you will an infection which is capable of eating through your skull which if left untreated will kill you by devouring your brain as well. The difference with this new MRSA is the speed at which it attacks the human body. And even worse is the idea that can get it from your local environment.
If this isn't bad enough a new virus has appeared in India that shares some of the characteristics of Dengue Fever and SARS: it is difficult to identify sharing many of the symptoms of Dengue Fever; it attacks adults not children, particularly young adults; it is characterised by sudden deterioration of condition within two days of the onset of fever and causing death through multi-organ failure.
Do any of these symptoms sound familiar - we might be looking at a new form of SARS if we are really unlucky.
So much for my plans to go to the beach this weekend. Sharks I can deal with (they all know me). Deadly flesh-eating bacteria is a whole 'nother story...
Looks like you got it wrong again, Jimbo! Sulfur content 'has been increasing'! - J. Reynolds
Obviously there is now an opening for us rank and file both to defend the environmental benefits of air pollution.. what about some comment on whether the "air pollution is good" line is utilisable, perhaps in rallies? - Wayne Hall
What we're able to do now is inadvertent.- Patrick Minnis, NASA
Is flesh-eating bacteria really as scary as the new movie makes it seem? Popular Science investigates.
by Tahalia Barrett
Cabin Fever, a thriller that explores the fear associated with necrotizing fasciitis—more commonly known as flesh-eating bacteria—is hitting theaters this week. In the movie, teens in a remote cabin (where else?) begin to turn on each other after one of them contracts the bacteria, with predictable results. But is the truth of the disease as scary as the movie? We spoke with James Musser, Chief of the Laboratory of Human Bacterial Pathogenesis at the National Institute of Allergy and Infectious Diseases, Dennis Stevens, Chief of Infectious Diseases at Boise Veteran's Affairs, and Victor Nizet, an Associate Professor of Pediatrics for the Division of Infectious Diseases at the University of California, San Diego, about what is known—and not known—about the bugs that eat your skin.
Popular Science: Cabin Fever is a movie about young adults vacationing in a cabin in the woods who confront the terror of having to kill to avoid infection when one of them develops necrotizing fasciitis. How does one get contract the disease?
Dennis Stevens: [Necrotizing Fasciitis] is actually caused by a bacterium—Group A Streptococcus—not a virus. It's necessary to have Group A Streptococcus in the environment but not sufficient. In the big picture, the likelihood of getting necrotizing fasciitis is remote unless you were all cut up.
PS: Who typically gets necrotizing fasciitis?
Victor Nizet: In the last decade we've seen a large increase in reports occurring in otherwise healthy children and adults. Although we see it in a wound, after surgery, or a cut or a scrape, up to 50 percent of people infected [with necrotizing fasciitis] don't have any wound or known complication. For many it's their first serious medical problem. That's one of the frightening things about it.
PS: What are the symptoms of the disease?
James Musser: There's no one single sign or symptom, just a general bad feeling of malaise and flu-like symptoms. It's a low frequency disease with nonspecific symptoms. Initial diagnosis is commonly missed early on.
VN: Sometimes the pain is out of proportion to what you see going on in the skin. I've seen it everywhere there's flesh: face, eyes foot, hands, abdomen. It could be misdiagnosed as appendicitis if in the abdomen or a heart attack if in the chest when what you really have is an infection spreading beneath the skin.
PS: How contagious is it?
VN: You and I have probably had the potentially dangerous necrotizing fasciitis-causing bacteria in our throats. Washing your hands when you're around anyone with strep is prudent, but risk of outbreaks spreading from person to person as indicated in this movie, there are few examples of that in actual medical experience.
PS: How quickly does it spread?
VN: If you have necrotizing fasciitis you have a life threatening condition that could spread to kill you within hours. Once you have it you can go from swollen calf to death's door within a period of days.
JM: When necrotizing fasciitis is recognized it's usually pretty far along. It can spread about an inch every couple of hours in its most fulminant form.
PS: You are caught in a cabin with necrotizing fasciitis. What do you do?
VN: What a surgeon would do is debreed [remove] the necrotic tissue. If you are of the same mindset as that guy who was caught in the woods and cut off his arm, you could perform your own amputation. That might buy you a little time.
Sports teams warned about unique skin infection By Gary Mihoces, USA TODAY
Concern is growing within the sports world and medical community over a bacterial skin infection resistant to usual antibiotics that flourishes in an athletic environment.
Recent cases on high school, college and pro football teams have been reported from Wisconsin to California to Texas to Florida. Those hospitalized included Miami Dolphins star linebacker Junior Seau, according to Florida newspapers.
A report by the national Centers for Disease Control and Prevention cited cases on a Colorado fencing team and an Indiana wrestling team.
According to the CDC, the bacteria is spread in ways that come with the territory in sports, including contact with infected persons or by contact with shared towels or equipment that carry the bacteria. The infection develops in routine cuts and scrapes.
"This is more of a beginning than a blip," says Bill Wucherer, health officer for Franklin, Wis., where eight high school football players were infected.
On Monday the National Collegiate Athletic Association issued an "alert on skin infections" to schools. The National Federation of High School Associations says it will send a similar alert this week to state high school sports bodies.
In August, the medical and training staffs of every National Football League club were sent copies of a CDC report about infections in sports related to the bacteria called methicillin-resistant staphylococcus aureus (MRSA).
"It's up to the physicians to be aware of it and respect the fact it could happen," says Elliot Pellman, team physician of the NFL's New York Jets.
Cases had been associated with patients in hospitals.
"Now we're seeing it emerge in settings where people have little or no contact with health care and are generally healthy. ... Sports teams are just the last couple of years," says Jeff Hageman, an epidemiologist with the CDC in Atlanta.
The CDC links the trend to the growing increase in resistance to antibiotics, but while MRSA is resistant to commonly used penicillin-related antibiotics, the CDC says the infections are treatable with other antibiotics.
Because it is not a typical staph infection, MRSA must be identified through tests of culture samples. Wounds accompanied by fever, swelling, redness and oozing are suspect as are boils.
Atlanta-AP -- A hard-to-treat skin infection common to hospitals and prisons has spread to schools in Georgia.
Health officials in the state are warning schools and their athletes about the staph infection. It has been found in recent years in several schools across the country, including some in Wisconsin, California, Indiana, Pennsylvania and Colorado.
The infection can't be cured by the usual penicillin-related antibiotics.
Though usually mild, the infection can progress to a life-threatening blood or bone infection.
Several athletes in Georgia have been hospitalized with the infection.
It can look like an ordinary skin wound or a boil and is often not diagnosed -- or ends up being treated with antibiotics.
Did you know that the moggy that sits on your lap, destroys the furniture and menaces the birdlife could actually kill you withou even trying - read on:
Cats 'can catch and pass on Sars'
Medical researchers have found cats can catch Sars and pass it on to other animals.
A team of US scientists at the University of Texas Medical Branch in Galveston say the finding raises the question of whether cats can pass the virus to humans.
Researcher Dr Robert Shope, an expert on emerging diseases, said: "You might want to quarantine the pets as well as the people. If it's been shown that the virus can transmit from cat to cat, it doesn't take much of a leap of faith that it will transmit to humans."
However, other scientists who have studied Sars say pet owners shouldn't overreact. The World Health Organisation's chief Sars scientist, D. Klaus Stohr, said: "These animals in all likelihood did not play a significant role in the spread of Sars to humans."
The Galveston researchers - whose study appears in the journal Nature, inoculated six cats and six ferrets with the virus cultured from a person who died of Sars, adding drops that contained the virus into their trachea, eyes and nose.
The cats and ferrets began to show their infection two days later in excretions from the throat, and researchers found they produced antibodies within 28 days. When the animals were later put down, the virus also was found in their respiratory tract.
The cats did not appear to be affected by the virus, but they did develop a mild case of pneumonia. The ferrets became lethargic, and one of them died four days after it was inoculated. Scientists also placed two healthy cats and two healthy ferrets with the infected animals.
The healthy ferrets showed signs of Sars infection after two days. The ferrets became emaciated and eventually died about two weeks later, though Osterhaus said he is uncertain whether this was due to the virus.
The virus seems to be so versatile that it could have jumped to humans from a variety of animals, co-author Albert DME Osterhaus said. The study also notes a separate report that cats were found infected with the virus in a Hong Kong apartment complex where residents contracted Sars last year.
The origin of the virus that killed 774 people remains unknown. In China exotic imported animals like raccoon-dogs and ferret badgers have been found harbouring a germ that's almost identical. The exotic animals were taken off the market for several months, but some have reportedly begun selling them again.
UPDATE on cats as SARS carriers - list also includes ferrets:
Cats, ferrets may be reservoir for SARS Last Updated Thu, 30 Oct 2003 10:27:26
ROTTERDAM, THE NETHERLANDS - Scientists have added pet cats and ferrets to the list of animals that can harbour the SARS coronavirus.
In laboratory experiments, researchers found domestic cats and ferrets can be infected with SARS taken from a human patient.
The animals transmitted the virus to uninfected animals housed with them, but scientists don't know if they can give it to people.
Dr. Klaus Stohr, the World Health Organization's chief SARS scientist, doubts domestic animals play a major role in spreading severe acute respiratory syndrome to humans.
Prof. Albert Osterhaus, a virologist at the Erasmus Medical Center in Rotterdam, found the animals can harbour the virus while he was testing potential drugs for SARS.
Osterhaus and his team reported the infected cats showed no clinical symptoms beyond a mild case of pneumonia. The ferrets became lethargic, and one died four days later.
In the study appearing in Thursday's issue of the journal Nature, researchers say they inoculated six cats and six ferrets by putting drops containing the virus into the animals' trachea, eyes and nose.
Throat secretions showed signs of the infection, and the cats and ferrets produced antibodies within 28 days, the researchers said.
Potential drug testing model The animals were later euthanized. Post-mortem tests showed the virus was in their respiratory tract.
Since the ferrets showed similar changes in their lungs to macaques infected with the SARS virus, Osterhaus says the domestic animals may be useful to test drugs and potential vaccines.
Virology experts say the study tested too few animals to conclusively say how cats and ferrets become infected.
Scientists don't know the origin of SARS, which killed 774 people.
In China, where the first outbreak began, exotic raccoon dogs, ferret badgers and civets were all found to be a reservoir for a SARS-like germ. The animals are considered a delicacy in China.
The WHO's representative in Beijing said markets took the animals off the shelves, but some have begun selling them again.
Last Updated: Sunday, 30 November, 2003, 00:09 GMT
A superbug with resistance to virtually all known antibiotics gained its power by hijacking genes from other bugs.
The strain, which was found in an ulcer on a diabetes patient, caused panic among the US doctors who found it.
More than 300 people who had come into contact with the elderly patient were tested to ensure it had not spread.
A report in the journal Science revealed that the bug had become dangerous because it had taken a gene from another bacterium in the ulcer.
There are many strains of bacteria which can resist modern antibiotics, with potentially lethal effects for the patients who catch them.
Staphylococcus aureus is carried by a high proportion of the population in their noses or on the skin, but can cause infections if they get into wounds.
While some strains are hard to treat because they resist certain antibiotics, doctors fear that even those used as a "last line of defence" will soon lose their potency.
There have been a number of reported cases of "vancomycin-resistant" Staphylococcus (VRSA) - signifying a strain which presents a high degree of resistance to conventional drugs.
The report in Science details a case in Detroit, which is unique because doctors were actually able to find the probable source of the mutation which turned a Staph infection with some antibiotic resistance into a "superbug".
The diabetic patient, from Detroit, had developed foot ulcers - a common complication of diabetes. These had become infected and were proving hard to treat with antibiotics.
Her doctor samples for analysis, which revealed that while most of the Staph bugs found were "only" resistant to some antibiotics, others could see off vancomycin as well.
This suggested that the change which produced the new bug may have actually happened on this patient, offering a golden opportunity to try to find out what had happened.
Experts at the Centers for Disease Control in Atlanta found traces of another bacterium, Enterococcus faecalis, which is common on hospitalised patients.
They found that the VRSA and this other bug shared some DNA - and a gene already known to help a bacterium fight vancomycin.
Further analysis revealed snippets of DNA - containing the gene, which were capable of "jumping" between different types of bacteria.
Fortunately, none of the 300 tests showed that the new bug had managed to spread.
Dr Donald Low, a clinical microbiologist at the University of Toronto, told Science: "We dodged another bullet."
The American Health Secretary, Tommy Thompson, has warned that the world is losing the fight against Aids.
Speaking in Zambia on World Aids Day, Mr Thompson called on the international community to intensify its efforts to combat the disease.
To mark the day, the United Nations unveiled ambitious plans to supply three million HIV sufferers with the drugs they need by the end of 2005.
An estimated 40 million people are now infected with HIV around the world.
According to the UN's World Health Organization (WHO), six million people in developing countries need anti-retroviral drugs, but less than 300,000 actually receive it.
The new strategy, called the "3x5" plan, will make cheaper drugs more available and simplify treatment regimens for millions of HIV sufferers as part of a two-year plan costing $5.5bn.
Launching the campaign in the Kenyan capital, Nairobi, WHO assistant-director General Jack Chow said HIV/Aids had become "the premier disease of mass destruction".
"It is inexorably converting developing nations into Aids-imploding nations."
In Zambia, one of the worst-hit nations, the US health secretary appealed for a redoubling of efforts to fight the disease, which is being carried by an estimated 26.6 million people in sub-Saharan Africa alone.
"We appear to be losing the fight against Aids at the moment," said Mr Thompson.
"We need America, the European Union and everybody. Nobody is going to be spared unless we all come together in the fight against this disease."
World leaders and millions of people around the world have highlighted the day with a series of events and planned activities.
* Former South African President Nelson Mandela urged the world to fight against the stigma associated with HIV, warning that "Many will die because of feeling less than human"
* Chinese Prime Minister Wen Jiabao made an unprecedented visit to people with Aids in a Beijing hospital
* UK Prime Minister Tony Blair said in a newspaper article the world had a "moral duty" to unite to fight Aids
* The Vatican issued a five-page statement, defending its opposition to condoms and stressing the importance of "fidelity, chastity and abstinence"
* In a rare admission, Saudi Arabia said there are nearly 7,000 Aids cases in the kingdom and announced a national strategy to combat the disease
* In Singapore, scantily-clad women handed out free condoms
* Sports stars and actors spearheaded an Aids awareness campaign in India, while thousands of students joined a "walk for life" rally in Delhi
* Hundreds of gay men and their families held a march in the Indian city of Bombay (Mumbai), urging the government to repeal a law banning sex between members of the same gender
* Some of Thailand's leading pop stars staged a free concert in Bangkok to raise Aids awareness
* In Cambodia, thousands of people sporting T-shirts with Aids slogans attended an Aids rally in the capital, Phnom Penh, before taking buses to the countryside to spread anti-Aids messages
* In Malaysia, the daughter of former Prime Minister Mahathir Mohamad, launched an Aids exhibition, warning about an alarming "level of denial" of the disease in her country
* In Albania, which has registered little more than 100 HIV cases in the past 10 years, high school students marched through the capital with candles and a banner reading "Protect Yourself and Others"
* In Europe, planned events included candlelight vigils in British cities and the Swedish capital, Stockholm, and workshops and rallies in Turkey and Portugal
* Activities were also planned across the Caribbean and Latin America, which hosts a world Aids conference for the first time on Tuesday
Last week's report from UNAids and the WHO warned that the disease was still spreading.
It said many countries were on the verge of fresh epidemics.
The number of reported infections is rising sharply in China, India, Indonesia and Russia, mostly due to HIV transmission through injecting drugs and unsafe sex.
The 3x5 campaign is being spearheaded by three United Nations agencies - the WHO, UNAids and the Global Fund to fight Aids, TB and Malaria.
Peter Piot, executive director of UNAids, said ensuring people have access to drugs is the only way to fight the disease, which he called a "global emergency".
He said only 75,000 HIV-infected Africans were getting treatment - out of the four million who need it.
"That is really not acceptable and we have no chance of halting this epidemic if we're not going to make sure that everybody who needs it has access to treatment."
UN Secretary General Kofi Annan warned that targets to fight HIV/Aids spelt out in the 2001 Declaration of Commitment are being missed.
"The epidemic continues its lethal march around the world, with few signs of slowing down," he said.
"We must work even harder to match our commitment with the necessary resources and action."
This article explains in part certain aspects of how viruses spread in the human body:
Scientists Solve Puzzle Of How Kinesin Motor Molecules Walk – Or Limp – Across Cells Source: Stanford University Date: 2003-12-08
Biophysicists at Stanford University have finally answered one of the most fundamental questions in molecular biology: How does the tiny motor molecule, known as kinesin, move across a living cell? According to the researchers, the solution to this longstanding problem will provide new insight into how motor proteins function, and may open new avenues of investigation for the treatment of cancer and various neurodegenerative diseases, such as Alzheimer's and Huntington's.
The study, published in the Dec. 4 online edition of the journal Science, was co-authored by Steven M. Block, a professor of applied physics and of biological sciences at Stanford.
"Motion at the cellular level is a hallmark of being alive," Block said. "A fundamental question is, how did living organisms figure out how to move? The answer is they developed kinesin and several other very efficient protein motors. If kinesin were to fail altogether, you wouldn't even make it to the embryo stage, because your cells wouldn't survive. It's that important."
Discovered in 1984, kinesin is now recognized as the workhorse of the cell, hauling chromosomes, neurotransmitters and other vital cargo along tiny molecular tracks called "microtubules." Many types of kinesin and kinesin-related proteins have been discovered in the past two decades in a wide range of organisms – from yeast to humans.
"Kinesin functions like a locomotive in cells to ferry cargo back and forth," Block said. "In brain cells, for example, it grabs these tiny sacs called vesicles, which are loaded with neurotransmitters that are needed for neurons to function, and moves them very long distances along microtubules."
A mere three-millionths of an inch long, a typical kinesin molecule has a tail on one end that hauls the cargo and two globular heads on the other end that alternately grab the microtubule and pull the cargo forward. One head has to be attached to the microtubule at all times for kinesin to advance against loads. "It's like pulling yourself straight up a ladder with your arms," Block explained. "If you were to let go of both hands, you'd fall off and that would be it."
For more than a decade, Block's lab and others have been trying to figure out the precise details of how kinesin's twin heads move – a process researchers call kinesin walking.
"There are two competing models for how kinesin walks: inchworm and hand-over-hand," Block said. "In the inchworm model, the leading head holds onto the microtubule, and the trailing head moves up to meet it. The second possibility is the hand-over-hand motion, which is more akin to the way we walk down the street, taking alternate strides every step."
In their experiment, Block and his colleagues used a specially designed microscope called the optical force clamp – a nanoscale instrument that allows researchers to watch a single kinesin molecule as it walks along a microtubule at rates up to about 100 steps per second. To their surprise, the researchers discovered that, instead of taking regular steps, kinesin actually walks with a limp.
"By 'limp' we mean that the timing of every alternate step is different than the one in between," Block said. "Suppose you have a sore leg that causes you to limp, and you have to walk across a river on stepping-stones, so you don't have any choice about where to put your feet. You don't want to spend a lot of time on the leg that's hurt, so you put it down and quickly get onto the other leg. As a result, the timing on every other step is short, whereas if you had two perfectly good legs, you'd spend equal time on each leg and your stride would be regular, not jerky."
This discovery provided an immediate solution to one part of the kinesin-walking puzzle.
"As soon as we saw limping, we said, 'Ah-hah!'," recalled Charles L. Asbury, a postdoctoral fellow in the Block lab and lead author of the Science study. "It's impossible for an inchworm to limp, because one head is always in the lead. Therefore kinesin must be using a hand-over-hand movement when it walks."
What's causing it to limp? "We're not sure," Block said, "but we speculate that maybe kinesin's coiled neck is getting over-wound and under-wound a little bit every time it takes a step."
Symmetry vs. asymmetry
The discovery of the hand-over-hand movement led the researchers to try and tackle another unanswered question: Is there symmetry in the way kinesin walks?
"It turns out that there are actually two kinds of the hand-over-hand models – asymmetric and symmetric," Block explained. "A normal human walk is asymmetric, because one leg always ends up in front of the other one, so at the end of each step, I'm in a different – that is, asymmetric – position relative to the axis of my body. In symmetric walking, I'm in the same geometry at the end of every step."
An example is a compass with a pencil on one arm that's used to mark off distances on a map. If you "walk" the compass in a line along a sheet of paper by rotating one arm in front of the other, the compass always ends up in the same symmetry after each step.
"But limping, by definition, means that every other step has to be different," he added. "That means kinesin's movements have to be asymmetric, so we can reject both the inchworm model and the symmetric hand-over-hand model."
The kinesin-microtubule system has been implicated in several serious diseases, which is one reason why medical researchers are particularly interested in understanding the fine details of how kinesins walk across microtubules.
"A number of diseases – such as Huntington's and Alzheimer's - involve proteins glomming together in the cell in ways that they shouldn't," Block said. "The cell tries to get rid of these bad protein aggregates by transporting them elsewhere using motor molecules such as kinesin. If we could understand something about how protein transport is done right, then maybe we could learn something about how it's done wrong. It may be possible to develop therapies that block the kinsein motion and prevent bad things from happening. In the future, it may even be possible to develop less toxic therapies that target specific kinesins in cancer cells, without damaging the healthy ones."
For example, taxol, a drug commonly used to treat breast cancer, works by stabilizing the microtubules that kinesins walk along and preventing them from de-polymerizing, Block noted.
Recent studies also have shown that certain viruses, including smallpox and herpes, infect cells by hitching a ride on kinesin, added Adrian N. Fehr, a graduate student in applied physics at Stanford and co-author of the Science study. "Normally, kinesin moves cargo from one part of the cell to another," he said. "But certain viruses have chemical receptors that kinesin recognizes, which enables them to hijack the kinesin and get a free ride through the cell."
The study was funded by the National Institute of General Medical Sciences and Stanford University.
Successful vaccination programmes against smallpox and polio, between 1950 and 1970, led to a general view by public health authorities, particularly in the West, that the war against infectious diseases was effectively over and some countries scaled-back health measures. The emergence of HIV and multi-resistant organisms has shown that constant vigilance is needed where micro-organisms are concerned.
The increase in incidence of known viral diseases, together with new infectious agents, depends upon a complex interaction of factors. These factors include the basic biology of the viruses, such as whether it has a linear or segmented genome, host and cell tropism, the route of transmission, the natural host reservoir and the vector. Within the past 50 years, changes in climate and habitats, social behaviour, urbanization, air travel and political instability has meant that emerging pathogens are able to traverse the globe more quickly than ever before.
HIV is the most notable example of an emerging virus, and since the syndrome was first noted in 1979 about 40 million people have been infected worldwide. In some African countries, half the adult mortality is attributable to HIV infection. In the USA, there have been more than half a million AIDS cases, and about one million people have been infected. Although combination therapies, available to Western countries, have reduced the incidence of HIV infections, perinatal transmission and death rates, new cases are increasingly associated with heterosexual contact.
The prevalence of hepatitis C virus worldwide is estimated at 3% of the world’s population. The full burden of this pandemic has yet to be experienced, since infection invariably leads to liver cirrhosis and hepatocellular carcinoma. The natural history of HCV has still to be fully understood, since sexual and vertical transmission are infrequent and transfusion with infected blood may constitute the biggest risk.
Yellow fever caused by another flavivirus, produces a haemorrhagic-like illness with a high mortality. It has recently seen a resurgence, and about 200,000 cases occur each year in Africa alone, of which a large proportion are children. With tropical mosquito species extending their range further northwards, it is likely that yellow fever may be introduced into both the southern states of the USA and southern Europe in the years to come.
In 1993, in the USA, a new hantavirus (sin nombre virus) was found to be the cause of an acute respiratory disease, termed hantavirus pulmonary syndrome (HPS), with high mortality in infected individuals. These viruses are usually transmitted by the inhalation of dried rodent faeces, urine or saliva, and with HPS the animal host was identified as the deer mouse. Molecular and serological surveys have revealed that related viruses causing HPS exist throughout the Americas.
Two new zoonotic viruses have been discovered in Australia. Several horses were killed by Equine morbillivirus in 1994, and, in separate incidents, three individuals working with the horses were infected and two died of respiratory failure and encephalitis. The Australian flying fox is the suspected natural host. In 1996, a lyssavirus was isolated from Australian flying foxes and other bats, and a zoo attendant became infected and died of encephalitis. These are rare events but it is unknown whether unrecognized cases have occurred in the past.
The explosive outbreaks and high mortality (50–90%) of Ebola virus (filovirus) have gained this virus worldwide attention. The natural reservoir of the virus remains unknown, but an arboreal host is suspected. Unrecognized infection and direct contact with infected blood and secretions can lead to rapid dissemination of the disease to family and healthcarers. But barrier nursing, isolation and contact tracing will contain the outbreak.
Another re-emerging virus is monkeypox, which is related to and produces a similar illness to smallpox. Its prevalence was rare during the period of widespread vaccination for smallpox, which provided protection against both viruses. A recent outbreak occurred in Zaire in 1997. There were at least 150 cases, of which 75% were children. The mortality rate was 3%. Person-to-person transmission was about 73%, which was much higher than in the previous outbreaks (30%), thus raising the concern of maintenance of monkeypox in human populations. The information being collated about emerging infections highlights the need for worldwide surveillance and response networks throughout the regions most at risk. There is also a requirement for an increase in basic research in identifying and characterizing emerging viruses, so that novel vaccines and drugs can be developed more quickly to reduce the impact of emerging infections.
The cloning and development of molecular assays used in identifying hepatitis C virus, in the absence of cell culture techniques, shows that the tools have long existed for identifying hitherto unknown virus infections. However, although many governments might complain about the cost of such surveillance and research, it must be emphasized that investment in this area will be cost-effective. It could be argued, for instance, that better surveillance in Africa might have reduced the impact of the AIDS epidemic.
Virus Distribution Disease Factors in transmission/emergence Year identified
Arboviruses Fever associated with myalgia, epigastric pain, nausea, diarrhoea and prostration
Yellow fever virus Africa, S. America Mosquito bite (monkey, humans)
West Nile virus Africa, Middle East, Europe Mosquito bite
Crimean-Congo haemorrhagic fever virus Africa, Middle East, Asia Tick
Australian bat lyssavirus Australia Encephalitis Bat handling bite 1996
Ebola Africa Haemorrhagic fever Unknown host, encroachment on host habitat, person-person transmission 1977
Enteric viruses Gastro-enteritis and acute diarrhoeal disease
Hepatitis A virus,
Hepatitis E virus Worldwide, greater in developing world Faecal—oral: poor hygiene, sanitation, food preparation
Equine Morbillivirus Australia Acute respiratory illness Contact with horses possibly infected by bat host 1994
Guanarito virus Venezuela Haemorrhagic fever Human activities leading to inhalation of excreta from rodent host 1991
Hantavirus (Sin Nombre prototype) Southwest USA Haemorrhagic fever with renal syndrome Inhalation of infected excreta from rodent host farming, increase in rodent numbers caused by favourable climatic conditions 1977
Hepatitis C Worldwide Cirrhosis of the liver and cancer Blood-borne, sexually and vertically transmitted, IVDU, unscreened blood transfusions, sexual behaviour 1989
Hepatitis G Worldwide Hepatitis Blood-borne, sexual transmission reported, disease association unclear, closely associated with HCV 1995
HIV Worldwide AIDS Blood-borne, sexually and vertically transmitted, IVDU, unscreened blood transfusions, sexual behaviour 1983
HSV-2 Worldwide Sexual transmission
HTLV-1 Worldwide, endemic in Japan and the Caribbean T-cell leukaemia Blood-borne, sexually and vertically transmitted, IVDU, unscreened blood transfusions, sexual behaviour 1980
HTLV-II Worldwide Unclear? Blood-borne, sexually and vertically transmitted, IVDU unscreened blood transfusions, sexual behaviour 1982
For some years now the involvement of viruses in human mental disorders has been considered, but never conclusively proven. The identification of Borna disease virus (BDV) as the infectious agent of neurological disease in many warm-blooded animals, has provided an opportunity to associate BDV with similar human diseases. Whilst the link currently remains unclear, one cannot dismiss the possibility that future treatment of psychiatric patients may involve antivirals.
Borna disease (BD) has been recognized as a rare neurological disease of horses for over 150 years. The name is derived from the town of Borna near Leipzig, Germany, where an outbreak was first reported. The virus, BDV, was first isolated from a horse in 1939, and is endemic to parts of Central Europe, although distribution is thought to be more widespread with cases reported in the US, Japan, Iran, Israel and New Zealand. It poses a sporadic threat to horses, its natural host, as well as sheep, cattle and an increasing number of domestic and zoo animals. Symptoms of Borna disease include severe viral encephalitis, with marked disturbances of movement and behaviour, followed by paralysis and then death. Mortality rates of 80-100% have been reported for diseased horses, thus providing a major challenge for veterinarians when outbreaks occur.
Although a viral aetiology has been accepted for over 60 years, the neurotropic BDV was only characterized in the last decade and emerged as the prototype enveloped, negative- and single-stranded RNA virus of the new family Bornaviridae, within the order Mononegavirales. The Mononegavirales also include Filoviridae (e.g. Marburg & Ebola viruses), Paramyxoviridae (e.g. mumps & measles viruses) and Rhabdoviridae (e.g. rabies & vesicular stomatitis viruses).
Viral transmission is assumed to occur through BDV-containing aerosols from salival, nasal and conjunctival secretions, although the exact nature remains unclear. Arthropods, such as equine ticks, have been discussed as potential vectors, but rodents provide a more likely candidate for both a natural reservoir and vector. In addition, sero-positive horses with sub-clinical disease are potential sources of infection for other animals and humans.
Borna viruses and human disease - fact or fiction?
The link between viruses and psychiatric disorders, although controversial, is not a new idea. As early as the 1920s Karl Menninger observed ‘dementia praecox’ or schizophrenia in post-influenza patients. More recently, other viruses such as Epstein-Barr, cytomegalovirus, herpes simplex, measles, mumps and rubella have also been implicated.
The broad host range of BDV, coupled with the fact that certain behavioural disturbances observed in animals were similar to human psychiatric disorders, such as manic depression, provided the opportunity to associate BDV infection with human disease. Early sero-epidemiological studies of psychiatric patients took advantage of the humoral immunity induced in response to infection, whereby BDV-specific antibodies were detected by serological techniques, such as indirect immunofluorescence, enzyme-linked immunoassays and Western blots. Some signs of BDV’s involvement in mental disorders were observed, with a BDV-specific antibody prevalence of 2-6%. A prospective study of 70 psychiatric patients by Liv Bode and colleagues, at the Robert Koch-Institut in Berlin, gave more convincing evidence, with an overall prevalence of 20%. Over 30% of patients with major depression were found to be antibody positive, compared to only 8% among patients with dysthymia (neurotic depression). Further evidence was provided when infectious BDV was isolated from the peripheral blood mononuclear cells (PBMCs) of three out of 23 psychiatric patients.
With the characterization of BDV in the 1990s and publication of viral sequence information, new diagnostic reagents were introduced, particularly oligonucleotide primers and probes for molecular epidemiology. Reverse transcriptase polymerase chain reaction (RT-PCR) and nested-RT PCR allowed rapid, sensitive detection of BDV transcripts from human PBMCs, and brain tissue. Groups in Germany and Japan detected viral nucleic acids in PBMCs of patients with various psychiatric diseases: Bode and colleagues found BDV nucleic acids in four (67%) of six patients, although larger studies observed a viral prevalence of 11-50%. Two studies in the US revealed BDV transcripts in 50 and 80% of post-mortem brain tissue, adding further support to the causal role of BDV. Significantly, many BDV-positive patients were diagnosed with schizophrenia, a severe psychiatric disorder affecting 1% of the general population, causing much excitement to virologists and clinicians alike.
Fuelling the controversy surrounding these positive findings, however, several research groups published contradictory data showing no association between psychiatric disease and BDV. In addition, BDV transcripts were detected in normal human brain tissue, suggesting that the virus could latently infect individuals with no clinical manifestations.
The potential for antiviral therapy
Whilst the exact involvement of BDV in psychiatric disorders remains unknown, the presence of BDV-specific antibodies and transcripts in patient samples cannot be ignored. Discrepancies between research groups may reflect differences in clinical populations, as well as assay sensitivities between laboratories. Thus, establishing generally accepted standards for diagnosis should ensure the questionable association is clarified. If the link between BDV and psychiatric disorders is proven, the prospect of antiviral intervention for such diseases as schizophrenia may become a reality.
Already the search for antiviral drugs has begun, and researchers who are firm believers in BDV and psychiatric disease association, such as Liv Bode and colleagues, are optimistic for their use in neurological therapeutics.
In 1997, Bode’s group reported the first use of the antiviral amantadine for the treatment of BDV-associated manic depression. Striking evidence was presented, with clearance of viral protein and RNA from the PBMCs of a patient, as well as alleviation of symptoms, in response to treatment. Whilst this study caused much excitement, sceptics argued that although amantadine had a possible role in the treatment of depression, the study did not confirm a viral aetiology in psychiatric disease. The well-known use of amantadine in the successful treatment of Parkinson’s disease implied psychotropic, but not necessarily specific anitiviral activity. Moreover, several studies by other groups failed to confirm an antiviral effect of amantadine with other BDV isolates in infected cells, rodents or horses. The use of amantadine in BDV-positive chronically depressed patients was revisited in 1999, and a therapeutic response of over 60% was observed. However, the issue of BDV involvement was questionable in some of the responders.
In a further effort to identify additional antiviral agents for BDV, Ian Lipkin’s group in the US performed in vitro inhibition experiments on several strains, and the nucleoside analogue ribavirin was shown to significantly reduce viral load. However, It remains to be seen whether this antiviral will be applicable in vivo.
There is no doubt that BDV infects humans, but the questions of viral prevalence and, most importantly, significance of these factors remain unanswered. The finding of traces of viruses or viral activity in the brain is no real proof of viral involvement in neurological disease and much work is needed before an association is confirmed.
Nevertheless, the establishment of a BDV connection with psychiatric disease provides tangible future applications – the potential use of specific antivirals and development of vaccines giving renewed hope to desperate patients. The riddle remains to be solved.
"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."
Latest research suggests an ingredient of Garlic will defeat MRSA:
Garlic beats bugs, no sweat
December 29, 2003
An ingredient in garlic may offer one of the best defences against hospital superbugs, new British research has shown.
The compound is said to be effective even against highly resistant strains of the notorious MRSA bug, which has claimed many lives.
It could cure patients with MRSA-infected wounds "within days", said Ron Cutler, a microbiologist at the University of East London who carried out the research. Allicin, which occurs naturally in garlic, also kills new superbug generations resistant to "last resort" antibiotics such as Vancomycin.
"MRSA is causing a genuine crisis in our hospital system in Britain and worldwide," Dr Cutler said.
"Antibiotics are increasingly ineffective, but we do have a powerful natural ally.
"Plant compounds have evolved over millions of years as chemical defence agents against infection. Garlic has been used in medicine for centuries, and it should be no surprise that it is effective against this very modern infection."
Evidence Of West Nile Turns Up In Baja Horses, Birds Show Antibodies To The Virus By Sandra Dibble Staff Writer San Diego Union-Tribune 1-2-4
TIJUANA -- Epidemiologists have found the first evidence of West Nile virus in Baja California, tracing antibodies for the disease to 16 horses across the state and six birds in the Mexicali area.
Although six human cases of the potentially deadly disease have been confirmed in Mexico, none has been in Baja California. The virus, carried by migratory birds, is transmitted to humans and horses by infected culex mosquitoes.
Because mosquito populations are down for the winter, the danger to humans at this time is "greatly reduced," said Dr. Jorge AcuÒa, an epidemiologist with the federal social security hospital in Mexicali.
But that scenario could change dramatically as spring approaches.
Some researchers are predicting a West Nile virus epidemic in Mexico because warm weather and tropical climates make many regions ideal breeding grounds for the mosquito.
But others say it is unclear how the disease will play out. They suggest that the presence in Mexico of another mosquito-borne disease, dengue fever, may have helped Mexicans build antibodies that will protect them from West Nile virus.
So far, the effects of the disease have been relatively benign in Mexico.
Since it was first identified in November 2002 in horses in the northern border states of Coahuila and Tamaulipas, federal health officials say just two horses and 10 birds have died from the disease.
In California, the first evidence of the virus was confirmed in mosquitoes near the Salton Sea in Imperial County in August. The state has since confirmed three human cases of the disease. The first was in Riverside County, the second in Imperial County and the third, confirmed Dec. 24, a 61- year-old man in Los Angeles County.
The discovery of animals carrying the disease antibodies in Baja California is "not surprising at all," said Dr. Steve Waterman, a medical epidemiologist with the U.S. Centers for Disease Control. "It confirms what people expected."
Dr. Alma Rosa M·rquez of the Baja California Health Secretariat said the six birds that tested positive for the virus were migratory, so it is unclear whether they became exposed to the virus in Baja California or elsewhere.
More details are expected later this month. The secretariat is awaiting the test results on native birds, although sentinel chickens placed around the state to detect the disease have shown no signs of being exposed, M·rquez said. Tests on mosquitoes also have been negative, she said.
With a statewide horse population estimated at 12,000, Baja California agriculture officials are closely following the virus. Eleven of the horses that tested positive for West Nile are in the Mexicali area, said Dr. Marco Antonio Vargas, head of animal health for the Baja California office of Mexico's federal agriculture secretariat. The remaining five are in Tijuana and Ensenada.
"The situation is as we had been expecting," Vargas said. "We have the same mosquitoes in Baja California as in California."
The agriculture secretariat has been urging horse owners to vaccinate their animals against the disease. Some of the horses could have tested positive because they had already received the vaccine, even though health officials have been trying to limit their tests to unvaccinated animals, Vargas said.
Baja California state health officials say they share information with California's Office of Binational Health. But Paula Kriner, an Imperial County epidemiologist, said local officials communicate only informally on the topic of West Nile virus.
"I'm hoping we can develop an exchange system," she said.
With the discovery of the Baja California cases, all six states on Mexico's northern border now show evidence of the virus, according to Mexico's National Center for Epidemiological Surveillance. Across the border from Texas, there were four human cases in Chihuahua and one in Nuevo Leon as of Dec. 25. A sixth case has been identified in the state of Sonora, but in a location far from the border.
In southern Mexico, 564 horses in the state of Chiapas had tested positive for antibodies to West Nile virus as of Dec. 25, more than in any other state in Mexico. But none had died as a result of the disease.
Group warns of spread of tumors among sea turtles in Japan
Members of the Osaka-based Sea Turtle Association of Japan warned on 29 Dec 2003 that a serious tumor-causing illness, called fibropapilloma, is apparently spreading among the turtles, with 3 cases found in Okinawa, Shizuoka, and Kochi prefectures since last summer. File photo shows a sea turtle in the sea near the Ogasawara islands, south of Tokyo.
Members of a Japan-based group working to protect sea turtles warned Monday that a serious tumor-causing illness is apparently spreading among the reptiles, with 3 cases having been identified in Japan since last summer.
The cases were found in Okinawa, Shizuoka and Kochi prefectures.
The illness, fibropapilloma, can be fatal when tumors block the turtle's mouth and eyes, obstructing the animal's movement and food intake. Experts believe the illness is caused by a virus.
A dead turtle found on Iriomote Island, Okinawa Prefecture, last summer had numerous tumors around the neck and legs and was diagnosed with severe fibropapillomas. Experts, however, could not determine the cause of death.
Another dead turtle was found on a beach in Omaezaki, Shizuoka Prefecture, in September with lesions on its legs. A 3rd turtle, still alive, was caught in a fishing net in November off Kochi.
Dr Akira Goto, who is gratefully acknowledged for forwarding the above articles, has also sent us the following 2 URL's with pictures of affected turtles, downloaded from the website of the Sea Turtle Association of Japan:
In 2000, a 4837-bp sequence of a newly found green turtle herpesvirus (GTHV), implicated in the etiology of green turtle fibropapilloma, was obtained by researchers at the Retrovirology Research Laboratory, Pacific Biomedical Research Center, University of Hawaii at Manoa, Honolulu, in 2000, from tumor tissues of a green turtle with fibropapilloma. See "Rapid acquisition of entire DNA polymerase gene of a novel herpesvirus from green turtle fibropapilloma by a genomic walking technique"; Yu Q, Hu N, Lu Y, Nerurkar VR, Yanagihara R.; J Virol Methods. 2001 Feb; 91(2):183-95. - Mod.AS.
"All truth passes through three stages. First, it is ridiculed, second it is violently opposed, and third, it is accepted as self-evident."
Arthur Schopenhauer, Philosopher, 1788-1860
"In the final analysis, our most basic common link is that we all inhabit this small planet, breathe the same air, and we all cherish our children’s future."