nsf.gov - National Science Foundation - Field fever, harvest fever, rat catcher's yellows: Leptospirosis by any name is a serious disease.- Campo de fiebre, cosecha en fiebre, recogedor de ratas amarillas, Leptospirosis por cualquier nombre es una enfermedad grave

Hola amigos:  A AVUELO DE UN QUINDE EL BLOG., hemos recibido información de la Fundación Nacional de Ciencias de Los Estados Unidos en que los científicos están estudiando la leptospirosis en la región de Los Ríos, en el centro-sur de Chile. Donde se presentas Ratas amarillas del colector, la fiebre del campo, fiebre cosecha, ictericia negro.Todos son nombres para la misma enfermedad, la leptospirosis, una infección causada por una bacteria con forma de sacacorchos llamada Leptospira.
Los síntomas varían de leves - dolores de cabeza, dolores musculares, fiebre - a condiciones más graves, como la meningitis y la hemorragia de los pulmones

Infection is more prevalent in lower-income tropical areas

Scientists are studying leptospirosis in the Los Rios region of south-central Chile. Credit and Larger Version

February 3, 2015

The following is part 14 in a series on the NSF-NIH-USDA Ecology and Evolution of Infectious Diseases (EEID) Program. See parts:one,two,three, four, five, six, seven, eight, nine, 10, 11, 12, and 13.

Rat catcher's yellows, field fever, harvest fever, black jaundice.

All are names for the same disease, leptospirosis, an infection caused by corkscrew-shaped bacteria called Leptospira.

Symptoms range from mild--headaches, muscle aches, fever--to more severe conditions, such as meningitis and bleeding from the lungs.

 

Looking for leptospirosis

 

"Leptospira bacteria are maintained through a complex transmission cycle," write scientist Claudia Munoz-Zanzi of the University of Minnesota and colleagues in a 2014 paper in the American Journal of Tropical Medicine.

"Humans and other mammals, domestic and wild, become infected after contact with urine from an infected host, or Leptospira-contaminated water or damp soil."

Some 7 to 10 million people contract leptospirosis each year. The disease is most prevalent in tropical areas, but may be found almost anywhere that's warm and wet.

In the developed world, leptospirosis occurs in people involved in outdoor activities, such as canoeing and kayaking in warm places. In developing countries, the disease largely happens to farmers and poorer people who live in cities.

Infection with Leptospira is linked with agricultural practices, fouling of household or recreational water, poor housing and waste disposal, and changes in the density or proximity of infected animals such as rodents, domestic animals like dogs and wildlife.

 

Rodents most common carriers

 

Rodents are the most common reservoirs of Leptospira, says Munoz-Zanzi.

With a grant from the National Science Foundation (NSF)-National Institutes of Health-U.S. Department of Agriculture Ecology and Evolution of Infectious Diseases (EEID) program, Munoz-Zanzi is studying the eco-epidemiology of leptospirosis.

Awards through the EEID program fund scientists to study how large-scale environmental events--such as habitat destruction and climate variability--alter the risks of viral, parasitic and bacterial diseases.

Munoz-Zanzi's goal is to improve knowledge of the social, epidemiological and ecological factors influencing leptospirosis in South America. She and colleagues are working to identify intervention strategies to reduce the disease's effect on the health of humans and other animals.

 

South-central Chile: a perfect home for Leptospira?

 

The study is taking place in the Los Rios region of south-central Chile. The area's climate is moderate, with an economy that's based on farming, agriculture, forestry and tourism.

Most of the region's human population is concentrated in a few urban centers, with the rest scattered in small towns or villages and farm areas.

Munoz-Zanzi's research involves contrasting leptospirosis in three community types: urban slums, rural villages, and farms.

Initial findings from the research showed that 20 percent of leptospirosis starts with rodents, including rats and mice, inside households and in other environments in populated areas.

Leptospira-carrying rodents turned out to be more abundant in rural villages than slums and farms.

"Social factors can be important causes of diseases," says Sam Scheiner, NSF EEID program director. "This study shows that the type of community can determine the presence of rats and mice that are disease-carriers. The results have implications for the control of many infectious diseases."
 

Danger in a puddle
 

"Because Leptospira live in water and soil," Munoz-Zanzi says, "the environment plays a key role in transmission in household pets, farm animals and people."

When the scientists collected water from puddles, containers, animal troughs, rivers, canals and drinking water, all showed contamination with Leptospira.

In households where puddles were found along with signs of rodent infestations, leptospirosis was common.

"However," says Munoz-Zanzi, "that was true only in lower income houses."

Some 19 percent of samples from these households--most from locations with warmer temperatures, and many with dogs as pets--tested positive.
 

Community setting important
 

The scientists are now examining leptospirosis in dogs and livestock, as well as in humans. They're integrating molecular, epidemiological and other data to gain insights into patterns of infection in various community types.

"The more we understand about this disease," says Munoz-Zanzi, "the more we realize the importance of the local community setting."

Ongoing efforts, she says, include the use of mathematical models to develop recommendations for disease control that's locally relevant. The scientists hope to provide people living in the most affected areas with tools to decrease the effects of leptospirosis.

In the meantime, how can people avoid contracting the disease?

"Wear protective equipment to prevent contact with potentially infected animals and environments," says Munoz-Zanzi, "wash after any such contact, and reduce rodents in places where people live and work."

Crowded tropical conditions where rats and mice freely run from house to house may herald another unwanted guest: Leptospira.

--	Cheryl Dybas, NSF (703) 292-7734 cdybas@nsf.gov

Related Programs Ecology and Evolution of Infectious Diseases

Related WebsitesNSF Special Report: Ecology and Evolution of Infectious Diseases: http://www.nsf.gov/news/special_reports/ecoinf/
NSF EEID Discovery Article Series:
 http://www.nsf.gov/discoveries/disc_summ.jsp?cntn_id=133576&org=NSF
NSF-NIH-USDA News: Racing ahead of disease outbreaks: $12 million in new research grants: http://nsf.gov/news/news_summ.jsp?cntn_id=132570
NSF Grant: Eco-epidemiology of Leptospirosis in Latin America: Understanding the Dynamics of Transmission Within a Community:
http://www.nsf.gov/awardsearch/showAward?AWD_ID=0913570&HistoricalAwards=false

Leptospira-carrying rodents are more abundant in rural villages than farms or slums.
Credit and Larger Version

Researchers collect water samples from puddles, containers, debris for Leptospira testing.
Credit and Larger Version

Field technicians prepare to place rodent traps inside and outside houses in a farm community.
Credit and Larger Version

For the study, biologists take samples from farms, villages and slums.
Credit and Larger Version

The disease culprits: Leptospira bacteria magnified.
Credit and Larger Versión
The National Science Foundation (NSF)
Guillermo Gonzalo Sánchez Achutegui
ayabaca@gmail.com
ayabaca@hotmail.com
ayabaca@yahoo.com
Inscríbete en el Foro del blog y participa : A Vuelo De Un Quinde - El Foro!

nsf.gov - Discovery - "Defective" Virus Leads to Epidemic of Dengue Fever

Virus may have led to widespread disease in Myanmar in 2001.-

 

Mosquitoes transmit the virus that causes the often-deadly disease dengue fever.
Credit: Wikimedia Commons
Download the high-resolution JPG version of the image. (1.2 MB)
 

Pagoda in Myanmar, site of a 2001-2002 epidemic of dengue fever.
Credit: Ruian Ke
Download the high-resolution JPG version of the image. (168 KB)
 

Map showing where dengue has occurred in the Eastern Hemisphere.
Credit: CDC
Download the high-resolution JPG version of the image. (81 KB)
 
The typical rash seen in people with dengue fever.
Credit: Wikimedia Commons
Download the high-resolution JPG version of the image. (9 KB)
 

Dengue is also on-the-march across the Western Hemisphere.
Credit: CDC
Download the high-resolution JPG version of the image. (67 KB)
 

Workers in the southern U.S. in the 1920s dig a drainage ditch to control mosquitoes.
Credit: Wikimedia Commons
Download the high-resolution JPG version of the image. (82 KB)

The following is part four in a series on the NSF-NIH Ecology and Evolution of Infectious Diseases (EEID) Program. For part one, please see: Cool Cat in a Hot Zone. For part two: Snails in the Waters, Disease in the Villages. For part three: Underwater Whodunit: What's Killing Florida's Elkhorn Coral?.

It's 2001 in Myanmar (formerly known as Burma), a country in Southeast Asia. Almost 200 people have died, and more than 15,000 are ill--all having contracted dengue fever.

Dengue is a disease transmitted by mosquitoes and caused by four types of dengue virus. Infection may not result in symptoms, or may cause mild, flu-like illness--or hemorrhagic fever.

Dengue virus infects some 50-100 million people annually in Southeast Asia, South America and parts of the United States.

In 1998, a pandemic of dengue resulted in 1.2 million cases of dengue hemorrhagic fever in 56 countries.

In Myanmar, dengue is endemic. The disease has occurred there in three- to five-year cycles since the first recorded outbreak in 1970. Each one has been more deadly.

What caused the widespread infection in Myanmar in 2001, a disease that resulted from one type of dengue virus, DENV-1? For more than a decade, researchers have been working to solve the puzzle.

All viruses not created equal

Could the DENV-1 in Myanmar have been different in some way, perhaps "defective"?

Defective viruses result from genetic mutations or deletions that eliminate essential functions. They're generated in viruses with high mutation rates, but were believed to be unimportant.

But it now appears that defective viruses may be able to play a critical role in the spread of disease.

In a paper published this week in the journal PLoS Pathogens, scientists funded by the National Science Foundation (NSF) report a significant link between one such defective virus and the high rate of transmission of DENV-1 in Myanmar in 2001.

"The idea has always been that defective viruses are either meaningless or detrimental," says James Lloyd-Smith, an ecologist and evolutionary biologist at University of California, Los Angeles.

"We've found the opposite--that the defective virus is actually helping the normal, functional virus. It's bizarre and hard to believe, but the data are the data."

"We've shown that the defective virus not only goes with the normal virus, but increases the transmission of that virus," says scientist Ruian Ke, also of UCLA.

While defective viruses can't complete their life cycle on their own, if they're able to get into the same cell with a non-defective virus, they can "hitch-hike" with the non-defective one and propagate.

Deadly outbreak of DENV-1

The research team--James Lloyd-Smith; Ruian Ke; John Aaskov, a virologist at Queensland University of Technology in Brisbane, Australia; and Edward Holmes, a biologist at the University of Sydney--found that the presence of a defective DENV-1 virus may have led to a spike in dengue fever cases in Myanmar during 2001-2002.

"The causes of epidemics are much more complicated than we thought," says Sam Scheiner, NSF program director for the joint NSF-National Institutes of Health Ecology and Evolution of Infectious Diseases (EEID) Program. At NSF, EEID is funded by the Directorates for Biological Sciences and Geosciences.

In addition to EEID, the research was supported by NSF's Advancing Theory in Biology Program.

"Pathogens can depend on the presence of other microbial species or, as in this case, other varieties of the same species," says Scheiner. "Understanding these interactions is critical for predicting when the next epidemic might occur--and how to prevent it."

In the study, Ke designed a mathematical model to learn how the defective DENV-1 virus interacted with the normal virus.

Aaskov and Holmes collected genetic sequences from the defective viruses from 15 people sampled over an 18-month period in Myanmar. All were infected with DENV-1 virus; nine were also infected with the defective version.

Ke discovered that the lineage of defective viruses emerged between June 1998 and February 2001; it spread through the population until at least 2002.

The following year, the lineage appeared in the South Pacific island of New Caledonia, carried there by a mosquito or a person.

The scientists analyzed the genetic sequences of the defective and normal viruses to estimate how long the defective virus had been transmitting in the human population.

"We can see from the gene sequence of the defective version that it's the same lineage, and is a continued propagation of the virus," says Lloyd-Smith.

"From 2001 to 2002, it went from being quite rare to being in all nine people we sampled that year," says Lloyd-Smith. "Everyone sampled who was getting dengue fever was getting the defective version along with the functional virus.

"It rose from being rare to being very common in just one year."

Most surprisingly, say the scientists, the combination of the defective virus with the normal virus was "more fit" than the normal dengue virus alone.

"What we've shown is that this defective virus, which everyone had thought was useless or even detrimental to the fitness of the functional virus, actually appears to have made it better able to spread," Lloyd-Smith says.

Ke calculated that the defective virus makes it at least 10 percent more transmissible. "It was spreading better with its defective cousin tagging along than on its own," says Lloyd-Smith.

It takes two (viruses) to tango

The functional virus and defective virus travel in unison. The two transmit together in an unbroken chain.

"That's not just a matter of getting into the same human or the same mosquito--they need to get into the same cell inside that human or mosquito in order to share their genes, and for the defective version to continue hitchhiking," says Lloyd-Smith.

"We're gaining insights into the cellular biology of how dengue is infecting hosts. It must be the case that frequently there are multiple infections of single cells."

The defective virus appeared one to three years before the major epidemics in 2001 and 2002.

"One could imagine that if you build an understanding of this mechanism, you could measure it, see it coming and potentially get ahead of it," says Lloyd-Smith.

Defective viruses: disease transmitters beyond dengue?

Might defective viruses play a role in the transmission of the flu, measles and other diseases?

"There are a few signs that this phenomenon may be happening in other viruses," Lloyd-Smith says.

"We may be cracking open the book on the possible interactions between normal, functional viruses and the defective ones that people thought were just dead-ends.

"These supposedly meaningless viruses may be having a positive effect--positive for the virus, not for us.

"There's great variation from year to year in dengue epidemics in various locations, but we don't understand why. This is a possible mechanism."

Why would a defective virus increase transmission of a disease?

Lloyd-Smith offers two hypotheses.

One is that the presence of the defective virus with the functional virus in the same cell makes the functional virus replicate better within the cell by an unknown mechanism.

"It might give the virus flexibility in how it expresses its genes, and may make it more fit and better able to reproduce under some circumstances," Lloyd-Smith says.

A second idea is that the defective virus may be interfering with the disease-causing virus, making the disease less intense.

People then have a milder infection, and because they don't feel as sick, they're more likely to go out of their homes and spread the disease.

In conducting the research, Lloyd-Smith and Ke combined genetic sequence analyses with sophisticated mathematical models and bioinformatics.

"We were able to show that this defective virus transmitted in an unbroken chain across this population in Myanmar for a year-and-a-half," Lloyd-Smith says.

"Without gene sequencing, we wouldn't have been able to establish that."

The biologists hope their work will help turn the tide of the next deadly outbreak of dengue in Myanmar--and in other tropical countries around the globe.

--	Cheryl Dybas, NSF (703) 292-7734 cdybas@nsf.gov

Related Websites
NSF Special Report: Ecology and Evolution of Infectious Diseases: 

http://www.nsf.gov/news/special_reports/ecoinf/index.jsp
PLOS Pathogens journal paper: 

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1003193
UCLA: defective dengue viruses: 

http://newsroom.ucla.edu/portal/ucla/defective-virus-surprisingly-243742.aspx
U.S. Centers for Disease Control and Prevention: Dengue:

 http://www.cdc.gov/dengue/

The National Science Foundation (NSF) 

 Guillermo Gonzalo Sánchez Achutegui

ayabaca@gmail.com

ayabaca@hotmail.com

ayabaca@yahoo.com

 Inscríbete en el Foro del blog y participa : A Vuelo De Un Quinde - El Foro!

nsf.gov - Discovery - Snails in the Waters, Disease in the Villages

Treatment for snail-borne schistosomiasis works best over the long haul.-

 Monitoring for infectious snails in bodies of water near villages in coastal Kenya.
Credit: J. Clennon, Emory University
Download the high-resolution version of the image. (104 KB)
Countries worldwide where people are at risk for the snail-borne disease schistosomiasis.
Credit: CDC
Download the high-resolution version of the image. (112 KB)

People who work in rice fields are exposed for many hours to snail-infested waters.
Credit: U. Kitron, Emory University
Download the high-resolution version of the image. (963 KB)

 
GIS map showing four communities in Kenya that are at high risk for schistosomiasis.
Credit: Charles King, Case Western Reserve University et al.
Download the high-resolution version of the image. (142 KB)  
 Diagnosis of schistosomiasis is made by detection of parasite eggs in urine samples.
Credit: C. King, Case Western Reserve University
Download the high-resolution version of the image. (178 KB) 
 Bulk containers of cans of pills of the anti-schistosomiasis drug praziquantel.
Credit: F. Richards, Carter Center
Download the high-resolution version of the image. (62 KB)

Watch where you jump in for a swim or where your bath water comes from, especially if you live in Africa, Asia or South America. Snails that live in tropical freshwater in these locations are intermediaries between disease-causing parasitic worms and humans.

People in developing countries who don't have access to clean water and good sanitation facilities are often exposed to the infected snails. Then they're left open to the parasitic worms.

The worms' infectious larvae emerge from the snails, cruise in shallow water, easily penetrate human skin and mature in internal organs.

The result is schistosomiasis, the second most socioeconomically devastating disease after malaria. As of 2009, 74 developing nations had identified significant rates of schistosomiasis in human populations.

There has been much debate about how best to prevent the disease, says Charles King, a physician and researcher at Case Western Reserve University in Cleveland, Ohio. "Beyond that," he asks, "how long should treatment last once someone has schistosomiasis?"

"Current guidelines focus on suppressing the disease's effects by limiting the infection during childhood," says King. "But that may not be enough to cure it or to prevent re-infection, leaving children still at risk for stunted growth and anemia."

King and colleagues recently published results of a study of long-term treatment of schistosomiasis in the journal PLOS Neglected Tropical Diseases.

The team's work is funded by the National Science Foundation (NSF)-National Institutes of Health (NIH) Evolution and Ecology of Infectious Diseases (EEID) program.

At NSF, the EEID program is supported by the Directorate for Biological Sciences and Directorate for Geosciences. At NIH, it's supported through the Fogarty International Center.

Schistosomiasis is usually treated with a single dose of the oral drug praziquantel.

World Health Organization (WHO) guidelines set forth in 2006 recommend that when a village reports that more than 50 percent of its children have parasite eggs in their urine or stool--a clear sign of schistosomiasis--everyone in the village should receive treatment.

When 10 to 50 percent of children are affected, say the guidelines, only school-age children should be treated--every two years. With less than 10 percent, mass treatment is not suggested.

But because of the long-term health effects of schistosomiasis, says King, "we now think it's better to provide regular yearly treatment."

He and scientists Xiaoxia Wang, David Gurarie and Peter Mungai of Case Western Reserve University; Eric Muchiri of the Ministry of Public Health and Sanitation in Nairobi, Kenya; and Uriel Kitron of Emory University in Atlanta, Georgia, used data collected in 10 villages in southeastern Kenya to run advanced models of village-level schistosomiasis transmission.

They scored the number of years each of the 10 villages would be projected to remain below a 10 percent infection level during a simulated 10-to-20-year treatment program.

All strategies that included an initial four annual treatments reduced community prevalence of the disease to less than 10 percent. Programs with gaps in treatment, however, didn't reach this objective in half the villages.

At typical levels of treatment, the researchers found, current WHO recommendations likely could not achieve full suppression of schistosomiasis.

"With more aggressive annual intervention that lasts at least four years," says King, "some communities might be able to continue without further treatment for 8 to 10 years.

"But in higher-risk villages, repeated annual treatment may be necessary for an indefinite period--until the eco-social factors that foster the disease [such as poor wastewater treatment] are removed."

In high-risk places, ongoing surveillance for the disease and annual drug treatment, the scientists say, need to become the mainstays of control.

In short, these villages require what they call "re-worming after de-worming."

But what happens if townspeople move to a more arid location, one with less freshwater and fewer snails?

In drier landscapes, schistosomiasis is a rare event that happens only during floods. Response to treatment therefore may be much better. Unless or until another flood occurs.

Although drier locales carry less risk for the disease, they're by no means free and clear. Even in arid locations, people would likely need to be treated more than once to get rid of the parasites.

"This research demonstrates the value of understanding where disease-causing organisms are in the environment," says Sam Scheiner, NSF program officer for EEID.

"Such knowledge can reduce human diseases much more effectively and at a lower cost than simply focusing on treatment."

The best goal, says King, is complete eradication of schistosomiasis.

To achieve that, scientists need to determine what makes a "wormy village," how often therapy is needed to prevent disease in such locations--and what can be done to change the environment such that a high-risk village becomes a low-risk one.

Related Websites
NSF Special Report: Ecology and Evolution of Infectious Diseases: 

http://www.nsf.gov/news/special_reports/ecoinf/index.jsp
NSF News Release: Controlling the Spread of Diseases Among Humans, Other Animals and the Environment:

 http://www.nsf.gov/news/news_summ.jsp?cntn_id=125496

 The National Science Foundation (NSF).

Guillermo Gonzalo Sánchez Achutegui

ayabaca@gmail.com

ayabaca@hotmail.com

ayabaca@yahoo.com

 Inscríbete en el Foro del blog y participa : A Vuelo De Un Quinde - El Foro!