A Kantele and TS Jokiranta Clinical Infectious Diseases, June 1, 2011; 52(11): 1356-62.
Human malaria has been known to be caused by 4 Plasmodium species, with Plasmodium falciparum causing the most-severe disease. Recently, numerous reports have described human malaria caused by a fifth Plasmodium species, Plasmodium knowlesi, which usually infects macaque monkeys. Hundreds of human cases have been reported from Malaysia, several cases have been reported in other Southeast Asian countries, and a few cases have been reported in travelers visiting these areas. Similarly to P. falciparum, P. knowlesi can cause severe and even fatal cases of disease that are more severe than those caused by the other Plasmodium species. Polymerase chain reaction is of value for diagnosis because P. knowlesi infection is easily misdiagnosed as less dangerous Plasmodium malariae infection with conventional microscopy. P. knowlesi infection should be suspected in patients who are infected with malaria in Southeast Asia. If human-mosquito-human transmission were to occur, the disease could spread to new areas where the mosquito vectors live, such as the popular tourist areas in western India.
Showing posts with label macaque monkey. Show all posts
Showing posts with label macaque monkey. Show all posts
Saturday, 16 July 2011
Tuesday, 3 May 2011
TUBERCULOSIS: Sequencing Study Finds Mutations in Latent Tuberculosis Bugs
April 25, 2011 By a GenomeWeb staff reporter
NEW YORK (GenomeWeb News) – An online study in Nature Genetics yesterday hints that drug resistance may arise in tuberculosis-causing bacteria even during latent stages of infection.
A Harvard University-led team sequenced the genomes of nearly three-dozen Mycobacterium tuberculosis isolates collected from nine infected macaques. When they used SNP data to gauge mutation rates at different stages of infection, the researchers found comparable levels of mutation under each of the conditions tested. The findings suggest drug resistance — including resistance to a treatment that relies on the antibiotic isoniazid alone — can likely occur even when tuberculosis infection is not at an active stage.
"We show that [M. tuberculosis] continues to acquire mutations during disease latency," senior author Sarah Fortune, an immunology and infectious diseases researcher with the Harvard School of Public Health, and her co-authors wrote, "which may explain why isoniazid monotherapy for latent tuberculosis is a risk factor for the emergence of isoniazid resistance."
Active tuberculosis is typically tackled with a combination of different antibiotics, the researchers explained. Latent infections, on the other hand, are considered less mutation prone, and are more often treated with a lone antibiotic called isoniazid, or INH.
Nevertheless, some epidemiological studies have reported elevated INH resistance in tuberculosis-causing bugs that had been treated with this preventative monotherapy, the authors explained, raising suspicions that mutations may be more common during latency than previously appreciated — a possibility that the team explored with whole-genome sequencing.
"[W]e sought to define the mutational capacity of the bacterium during infection to better predict the rate at which drug resistance can be expected to emerge in active, latent, and reactivated disease," they wrote.
Using the Illumina Genome Analyzer, the researchers did single-read and paired-end sequencing of a M. tuberculosis strain known as Erdman and of 33 M. tuberculosis isolates from nine macaques that either had active tuberculosis infections, latent infections, or infections that were re-activated after a period of latency.
In the process, they generated sequence that covered 93 percent of each genome, on average, to a depth of about 117 times.
After tracking down variants in the genomes and verifying them with targeted Sanger sequencing, the team was left with 14 SNPs that seem to have arisen over the course of macaque infections. But rather than seeing more mutations in the isolates from macaques with active tuberculosis infections, the researchers found comparable mutation rates in each of the three infection scenarios.
"Our data indicate that in macaques with active, latent, and reactivated disease, the bacterial populations acquire mutations at the same rate over time, regardless of the number of bacterial replications that have occurred," they wrote.
Moreover, their subsequent experiments hint that these mutation rates are similar to those found when M. tuberculosis is grown in a lab setting.
The findings suggest that drug resistance is not only an issue to contend with during active tuberculosis infection, the researchers explained, since bacteria can also mutate during latent infection and in early stages of reactivation.
Those involved in the study emphasize that more research is needed to understand whether M. tuberculosis mutation patterns are similar in infected humans. Still, they say, the results underscore the need for surveillance for resistance-related mutations — particularly if preventative INH treatment becomes more broadly used to treat latent tuberculosis in some populations, including those infected with HIV.
"[INH preventative monotherapy] is now being recommended globally for HIV-positive individuals with latent tuberculosis where bacterial burden and the rate of treatment failure may be higher because of immunocompromise," the authors noted.
"If our data from the macaque model are predictive of the mutational capacity of [M. tuberculosis] in HIV-positive individuals, INH mono-resistance could arise at a substantial rate," they added. "These findings emphasize the importance of drug resistance testing and careful monitoring for treatment in these populations."
http://www.genomeweb.com/sequencing/sequencing-study-finds-mutations-latent-tuberculosis-bugs
NEW YORK (GenomeWeb News) – An online study in Nature Genetics yesterday hints that drug resistance may arise in tuberculosis-causing bacteria even during latent stages of infection.
A Harvard University-led team sequenced the genomes of nearly three-dozen Mycobacterium tuberculosis isolates collected from nine infected macaques. When they used SNP data to gauge mutation rates at different stages of infection, the researchers found comparable levels of mutation under each of the conditions tested. The findings suggest drug resistance — including resistance to a treatment that relies on the antibiotic isoniazid alone — can likely occur even when tuberculosis infection is not at an active stage.
"We show that [M. tuberculosis] continues to acquire mutations during disease latency," senior author Sarah Fortune, an immunology and infectious diseases researcher with the Harvard School of Public Health, and her co-authors wrote, "which may explain why isoniazid monotherapy for latent tuberculosis is a risk factor for the emergence of isoniazid resistance."
Active tuberculosis is typically tackled with a combination of different antibiotics, the researchers explained. Latent infections, on the other hand, are considered less mutation prone, and are more often treated with a lone antibiotic called isoniazid, or INH.
Nevertheless, some epidemiological studies have reported elevated INH resistance in tuberculosis-causing bugs that had been treated with this preventative monotherapy, the authors explained, raising suspicions that mutations may be more common during latency than previously appreciated — a possibility that the team explored with whole-genome sequencing.
"[W]e sought to define the mutational capacity of the bacterium during infection to better predict the rate at which drug resistance can be expected to emerge in active, latent, and reactivated disease," they wrote.
Using the Illumina Genome Analyzer, the researchers did single-read and paired-end sequencing of a M. tuberculosis strain known as Erdman and of 33 M. tuberculosis isolates from nine macaques that either had active tuberculosis infections, latent infections, or infections that were re-activated after a period of latency.
In the process, they generated sequence that covered 93 percent of each genome, on average, to a depth of about 117 times.
After tracking down variants in the genomes and verifying them with targeted Sanger sequencing, the team was left with 14 SNPs that seem to have arisen over the course of macaque infections. But rather than seeing more mutations in the isolates from macaques with active tuberculosis infections, the researchers found comparable mutation rates in each of the three infection scenarios.
"Our data indicate that in macaques with active, latent, and reactivated disease, the bacterial populations acquire mutations at the same rate over time, regardless of the number of bacterial replications that have occurred," they wrote.
Moreover, their subsequent experiments hint that these mutation rates are similar to those found when M. tuberculosis is grown in a lab setting.
The findings suggest that drug resistance is not only an issue to contend with during active tuberculosis infection, the researchers explained, since bacteria can also mutate during latent infection and in early stages of reactivation.
Those involved in the study emphasize that more research is needed to understand whether M. tuberculosis mutation patterns are similar in infected humans. Still, they say, the results underscore the need for surveillance for resistance-related mutations — particularly if preventative INH treatment becomes more broadly used to treat latent tuberculosis in some populations, including those infected with HIV.
"[INH preventative monotherapy] is now being recommended globally for HIV-positive individuals with latent tuberculosis where bacterial burden and the rate of treatment failure may be higher because of immunocompromise," the authors noted.
"If our data from the macaque model are predictive of the mutational capacity of [M. tuberculosis] in HIV-positive individuals, INH mono-resistance could arise at a substantial rate," they added. "These findings emphasize the importance of drug resistance testing and careful monitoring for treatment in these populations."
http://www.genomeweb.com/sequencing/sequencing-study-finds-mutations-latent-tuberculosis-bugs
Saturday, 23 April 2011
MALARIA: Plasmodium knowlesi is transmitted between monkeys: 300 human cases per year
Joseph Milton : 13 April 2011
The parasite infects macaques, but it can also be transmitted to humans
Flickr/Michael Ransburg
Monkeys in Malaysian forests are a reservoir for a rare form of malaria that could become a significant cause of disease in humans throughout South-East Asia, a study warns.
The malaria parasite Plasmodium knowlesi is transmitted between monkeys by forest-dwelling mosquitoes. This limits transmission to humans and, at present, there are only around 300 human cases per year.
But as human populations grow and the forest shrinks, people are likely to venture into the forest more often and in greater numbers. This, said the researchers, could lead the parasite to evolve, enabling it to pass more easily between humans and monkeys.
Balbir Singh, director of the Malaria Research Centre at the University of Malaysia, Sarawak (UNIMAS), and colleagues first showed in 2004 that P. knowlesi causes deadly disease in humans. They did not know whether the disease is maintained in the human population or whether the monkeys act as wild reservoirs from which humans get infected.
Singh, who led the current study, published last week (7 April) in PLoS Pathogens, said he suspected macaque populations in Sarawak, Borneo, were a reservoir for P. knowlesi — and were the source of human malaria cases seen in local hospitals — as monkey populations in other areas are also known to act as malaria reservoirs.
Singh's team looked closely at the DNA of P. knowlesi in 108 wild macaques from Sarawak and 31 human malaria patients.
They found that the disease is maintained in the monkeys but that, as humans become increasingly exposed, it could switch host and adapt to infecting people. Macaques had multiple P. knowlesi infections, while most human patients had just one, and the parasite diversity was much higher in the monkeys, which could make it more difficult to eliminate the disease.
"These macaques are the most common non-human primate in the jungles of South-East Asia," Singh said. "It's a huge reservoir of parasites, so trying to eliminate malaria might be virtually impossible."
As deforestation and human populations increase, Singh fears the parasite could evolve, switching its preferred host to humans and leading to large-scale malaria outbreaks caused by the strain.
"Anything that brings humans into increasing contact with the forest could increase the risk," said Catherine Walton, an evolutionary biologist at the University of Manchester, United Kingdom.
Richard Coker, head of the communicable diseases policy research group at the London School of Hygiene and Tropical Medicine, United Kingdom, said population growth and deforestation would "continue to contribute to the emergence and spread of novel pathogens with increasing frequency".
http://www.scidev.net/en/news/malaysian-monkey-malaria-could-spread-in-humans-.html
The parasite infects macaques, but it can also be transmitted to humans
Flickr/Michael RansburgMonkeys in Malaysian forests are a reservoir for a rare form of malaria that could become a significant cause of disease in humans throughout South-East Asia, a study warns.
The malaria parasite Plasmodium knowlesi is transmitted between monkeys by forest-dwelling mosquitoes. This limits transmission to humans and, at present, there are only around 300 human cases per year.
But as human populations grow and the forest shrinks, people are likely to venture into the forest more often and in greater numbers. This, said the researchers, could lead the parasite to evolve, enabling it to pass more easily between humans and monkeys.
Balbir Singh, director of the Malaria Research Centre at the University of Malaysia, Sarawak (UNIMAS), and colleagues first showed in 2004 that P. knowlesi causes deadly disease in humans. They did not know whether the disease is maintained in the human population or whether the monkeys act as wild reservoirs from which humans get infected.
Singh, who led the current study, published last week (7 April) in PLoS Pathogens, said he suspected macaque populations in Sarawak, Borneo, were a reservoir for P. knowlesi — and were the source of human malaria cases seen in local hospitals — as monkey populations in other areas are also known to act as malaria reservoirs.
Singh's team looked closely at the DNA of P. knowlesi in 108 wild macaques from Sarawak and 31 human malaria patients.
They found that the disease is maintained in the monkeys but that, as humans become increasingly exposed, it could switch host and adapt to infecting people. Macaques had multiple P. knowlesi infections, while most human patients had just one, and the parasite diversity was much higher in the monkeys, which could make it more difficult to eliminate the disease.
"These macaques are the most common non-human primate in the jungles of South-East Asia," Singh said. "It's a huge reservoir of parasites, so trying to eliminate malaria might be virtually impossible."
As deforestation and human populations increase, Singh fears the parasite could evolve, switching its preferred host to humans and leading to large-scale malaria outbreaks caused by the strain.
"Anything that brings humans into increasing contact with the forest could increase the risk," said Catherine Walton, an evolutionary biologist at the University of Manchester, United Kingdom.
Richard Coker, head of the communicable diseases policy research group at the London School of Hygiene and Tropical Medicine, United Kingdom, said population growth and deforestation would "continue to contribute to the emergence and spread of novel pathogens with increasing frequency".
http://www.scidev.net/en/news/malaysian-monkey-malaria-could-spread-in-humans-.html
Friday, 8 April 2011
MALARIA: the monkey reservoir
8 April 2011 James Gallagher: Health reporter, BBC News
A type of malaria could move from monkeys to humans, say scientists
Macaques in south east Asia are a vast source of Plasmodium knowlesi which can spread to people, they write in PLoS Pathogens.
They believe that growing human populations and increased deforestation in the region could lead to the parasite switching host.
But those changes could also reduce the spread of the disease.
Around one million people die each year as a result of malaria.
It is caused by parasites and is spread by mosquitoes when they drink blood.
'Huge reservoir'
P. knowlesi is known as the fifth malarial parasite in humans.
It mostly exists in monkeys, however, there have been human cases and it has been shown in the laboratory to be able to spread from human to human.
With increasing human populations and deforestion we may get a shift to humans”
In south east Asia, the macaques are the second most common primate after humans.
Blood tests on 108 wild macaques showed that more than three quarters were infected with the malaria parasite.
Professor Balbir Singh, from the Malaria Research Centre at Universiti Malaysia Sarawak, told the BBC: "they are a huge reservoir of Plasmodium knowlesi."
Genetic analysis showed that P. knowlesi had existed in monkeys since before humans settled in south east Asia. The researchers said humans were being infected from the 'reservoir', rather than the disease spreading between humans.
Prof Singh raised concerns about what could happen in the future: "We don't know how mosquito behaviour will change.
"With increasing human populations and deforestation we may get a shift to humans. The number of malaria cases is coming down so there is also decreased immunity. Or would deforestation reduce numbers? It could go either way."
Dr Hilary Ranson, from the Liverpool School of Tropical Medicine, said: "It seems a very reasonable thing to speculate.
"Deforestation or any perturbation of the ecosystem frequently leads to humans being exposed to an expanded range of biting insects and the pathogens they transmit, yellow fever is a good example of this."
She said if humans catch the parastite more often then P knowlesi may evolve to target humans.
"To me the important message is that disruption of the environment exposes people to a range of known and potentially unknown pathogens transmitted by blood feeding insects that do not typically feed on humans" she added
http://www.bbc.co.uk/news/health-13001294
Macaques in south east Asia are a vast source of Plasmodium knowlesi which can spread to people, they write in PLoS Pathogens.
They believe that growing human populations and increased deforestation in the region could lead to the parasite switching host.
But those changes could also reduce the spread of the disease.
Around one million people die each year as a result of malaria.
It is caused by parasites and is spread by mosquitoes when they drink blood.
'Huge reservoir'
P. knowlesi is known as the fifth malarial parasite in humans.
It mostly exists in monkeys, however, there have been human cases and it has been shown in the laboratory to be able to spread from human to human.
With increasing human populations and deforestion we may get a shift to humans”
In south east Asia, the macaques are the second most common primate after humans.
Blood tests on 108 wild macaques showed that more than three quarters were infected with the malaria parasite.
Professor Balbir Singh, from the Malaria Research Centre at Universiti Malaysia Sarawak, told the BBC: "they are a huge reservoir of Plasmodium knowlesi."
Genetic analysis showed that P. knowlesi had existed in monkeys since before humans settled in south east Asia. The researchers said humans were being infected from the 'reservoir', rather than the disease spreading between humans.
Prof Singh raised concerns about what could happen in the future: "We don't know how mosquito behaviour will change.
"With increasing human populations and deforestation we may get a shift to humans. The number of malaria cases is coming down so there is also decreased immunity. Or would deforestation reduce numbers? It could go either way."
Dr Hilary Ranson, from the Liverpool School of Tropical Medicine, said: "It seems a very reasonable thing to speculate.
"Deforestation or any perturbation of the ecosystem frequently leads to humans being exposed to an expanded range of biting insects and the pathogens they transmit, yellow fever is a good example of this."
She said if humans catch the parastite more often then P knowlesi may evolve to target humans.
"To me the important message is that disruption of the environment exposes people to a range of known and potentially unknown pathogens transmitted by blood feeding insects that do not typically feed on humans" she added
http://www.bbc.co.uk/news/health-13001294
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