Scientists with the Health Protection Agency have developed a new test that can diagnose TB within one hour, the agency says. Data on the "ultra-rapid" test are being presented today at the University of Warwick at HPA's annual conference, Health Protection 2010.
Standard testing can take up to eight weeks to grow and identify TB bacteria. Other rapid molecular tests focus on an element in TB that, while normally occurring, is present in very low amounts or even lacking in some circulating strains, HPA said.
The experimental test is more sensitive, using real-time polymerase chain reaction to amplify copies of a piece of tuberculosis DNA and generate millions of that particular sequence. The test focuses on that single tuberculosis DNA molecule. To further evaluate the product, trials comparing it with standard tests are planned for UK labs during the next year.
"We're excited to have developed this new test because it means we can potentially diagnose someone at a TB clinic within an hour and start them immediately on the treatment they need," said Cath Arnold, study leader and head of HPA's genomic services unit. "This new test could really have an impact where it is needed most."
"Up to 75 percent of people with TB are transient, and it is difficult if they are not treated straightaway because they can move on and infect people," said Emma Gilgunn-Jones, an HPA spokesperson. It will likely be at least two years before the test is available on the market, she noted.
Thursday, September 16, 2010
"New Test Gives One-Hour TB Diagnosis: Scientists" Agence France Presse (09.15.10)
Thursday, August 26, 2010
Wednesday, August 11, 2010
China Takes More Aid Money for AIDS and Malaria than African Countries
Since its launch, the Global Fund to Fight AIDS, TB and Malaria has given China nearly $1 billion in grants. Despite this, few countries forced to compete for health grants with the world's second-largest economic power have voiced any opposition, according to Jack Chow. A former US ambassador on global HIV/AIDS, Chow was the lead US negotiator in the founding of the fund; his essay appeared in Foreign Policy magazine.
Although it is an economic powerhouse, China's low per capita income allows it to compete for grants with countries like Bolivia, Cameroon, and India, Chow said. China's aggregate award from the fund is nearly three times larger than that given to South Africa - one of the countries most affected by the diseases, Chow wrote.
At the fund's inception, "We imagined the bulk of the money ending up in places like Lesotho, Haiti, and Uganda, where these diseases have reached crisis levels," Chow said. China may value Global Fund grants as a means through which it can access technical assistance from international health agencies, he suggested.
Nonetheless, a grant system under which China is the fourth-largest recipient threatens to undermine Global Fund efforts to raise $13 billion to $20 billion for projects during 2011-13, Chow said.
China has made Global Fund contributions of $2 million annually, or $16 million during the last eight years, "but China has recouped its spending by 60 times," Chow wrote. In comparison, the United States has donated $6.5 billon and Britain has pledged $2.2 billion.
"China has won malaria grants totaling $149 million in a country where only 38 deaths from the illness were reported last year," wrote Chow. "That is more money than the Democratic Republic of Congo, which reported nearly 25,000 malaria deaths in the same period."
"For many of the poorer countries that lose out, opposing China in international forums would risk incurring Beijing's diplomatic wrath," Chow suggested.
The Telegraph (London) (08.05.10):: Malcolm Moore
Tuesday, August 10, 2010
Human Clinical Trial of NIH-developed Dengue Vaccine Begins
After more than a decade of development at the National Institutes of Health, a vaccine to prevent infection by the mosquito-borne dengue virus has begun human clinical testing. The vaccine was developed by scientists at the National Institute of Allergy and Infectious Diseases (NIAID) and is undergoing clinical study at the Johns Hopkins Bloomberg School of Public Health in Baltimore.
About 2.5 billion people in more than 100 countries worldwide live in areas where they are at risk of dengue infection. “This is an important milestone for NIAID’s intramural scientists in the development of a model dengue vaccine, which could potentially have a major impact in preventing dengue,” says NIAID Director Anthony S. Fauci, M.D. “With increasing infection rates and disease severity around the world and the discovery of dengue in parts of Florida, finding a way to prevent dengue infection is an important priority.”
Dr. Fauci is co-author of a 2008 commentary in the Journal of the American Medical Association that raised awareness of dengue as an emerging infectious disease.
Dengue fever is caused by any of four related viruses – DENV-1, DENV-2, DENV-3 and DENV-4 – which are transmitted to humans by Aedes mosquitoes. Dengue virus is prevalent in the tropical and subtropical regions of the world and each year infects about 50 million to100 million people. It accounts for 25,000 deaths annually, most of them in children.
Most people infected with dengue virus experience no symptoms at all or only a mild fever. Others develop flu-like symptoms, headache, and joint and muscle pain. A smaller portion of those infected experience the more severe dengue hemorrhagic fever/shock syndrome (DHF/DSS), which can cause high fever, pain, bleeding, a drop in blood pressure, and, in some cases, coma or death.
There is no vaccine to prevent dengue infection or drug treatment for those who become infected. Current treatment recommendations include bed rest, drinking fluids, and taking medicine to reduce fever. The only way to prevent infection is to avoid being bitten by Aedes mosquitoes. These mosquitoes are most active during the day and thrive in urban environments, two factors that make them difficult to avoid.
“Controlling the mosquito vector can work, but it is very expensive and difficult to sustain,” says Anna Durbin, M.D., who is leading the study at Johns Hopkins. “In the long run, vaccination would be a more efficient and cost-effective approach.”
The new vaccine is tetravalent, meaning that it is designed to protect against all four dengue viruses, also called serotypes. This is especially important because of the way the immune system responds. A person who develops antibodies against one serotype of dengue virus is protected against only that specific serotype. To be fully protected against the four forms of dengue, a person must have antibodies against all four serotypes of the virus. However, having some antibodies to dengue may be worse than having none: Someone who has antibodies against only one or a few of the virus serotypes is actually at higher risk of developing the severe form of the disease upon infection by another serotype. But a person who is immune to all four serotypes cannot be reinfected, and, therefore, is less likely to develop DHF/DSS.
Development of the vaccine was led by Stephen S. Whitehead, Ph.D., and Brian Murphy, M.D., of NIAID’s Laboratory of Infectious Diseases. The researchers started by testing seven monovalent vaccines, each of which is designed to protect against a single dengue serotype.
“Our overall strategy was to identify the best individual candidate for each serotype, based on safety and ability to induce an immune response, and to then combine those into a tetravalent vaccine,” explains Dr. Whitehead. To optimize the immune response to each dengue serotype, the researchers are testing three different candidate combinations of the four monovalent vaccines.
In this Phase I trial, study volunteers who have never been exposed to dengue were randomly assigned to receive one of the candidate tetravalent vaccine formulations or a placebo. The candidate vaccines are live-attenuated, or created by making the live virus harmless or less virulent.
Evaluation of a second candidate combination vaccine has been initiated at the University of Vermont in Burlington, and trials of the third candidate will begin shortly thereafter at Johns Hopkins. These early clinical trials are designed to test the vaccine’s safety and ability to stimulate immune responses in healthy adults ages 18 to 50. After a baseline assessment, participants will receive one dose of the assigned vaccine or placebo. At follow-up study visits over the next six months, the researchers will assess their health and dengue symptoms and collect blood and urine samples for analysis. After determining which tetravalent vaccine is most promising, the researchers will test that candidate in a trial in a new group of volunteers in Brazil, where dengue has become highly prevalent.
The next stage of testing, a Phase II trial, will involve more participants and will test for differences in preliminary signs of effectiveness between people who have been exposed to dengue and those who have not, as well as the need for a booster shot within a few months of the initial vaccination. “If everything goes well after that stage, we hope to start the final phase of human testing in three to four years,” says Dr. Durbin.
For more information, visit NIAID’s Dengue Fever Web portal.
###
References:
National Institute of Allergy and Infectious Diseases. NIAID scientists use reverse genetics to develop potential dengue vaccine.
DM Morens and AS Fauci. Dengue and hemorrhagic fever: A potential threat to public health in the United States. JAMA DOI:10.1001/jama.299.2.214 (2007).
SS Whitehead, JE Blaney, AP Durbin, and BR Murphy. Prospects for a dengue virus vaccine. Nature Reviews Microbiology DOI: 10.1038/nrmicro1690 (2007).
http://www.niaid.nih.gov/news/newsreleases/2010/Pages/denguevaxtrial.aspx
Sunday, August 8, 2010
Tuberculosis Breakthrough Announced (Canada)
Dr. Maziar Divangahi of McGill University and the Research Institute of the McGill University Health Center stated that there may be an opportunity to improve TB vaccination and treatment using existing drugs. He explained the process by which TB-causing bacteria enter the body through the oral cavity, and white blood cells or macrophages engulf and encapsulate, but are unable to kill the bacteria. The bacteria undergo a type of hibernation and propagate inside the engulfment until the macrophages can hold them no more. The macrophages break apart, allowing the spread of the infection in the body. Normally macrophages trap bacteria inside their cell membranes and the bacteria die slowly, but this does not work for TB bacteria. TB bacteria have a system called necrosis, which destroys cell membranes aiding the bacteria’s escape. Dr. Divangahi focused on exploring the use of elcosanoids. He noted that elcosanoids can work with or against macrophages in relation to TB bacteria. Analysis of human genes found that changes occurring in the presence of elcosanoids will either produce immunity or susceptibility to TB. Elcosanoid-producing drugs are available and are used in treating other inflammatory diseases. Dr. Divangahi predicted that the next steps will be to determine how these drugs can be used to treat TB.
News Fire, www.news-fire.com, July 30, 2010, by Robert Valenzuela
Friday, August 6, 2010
Neuropathic pain in diabetes—evidence for a central mechanism
Tanya Z. Fischer & Stephen G. Waxman
Hyperexcitability of and aberrant spontaneous impulse generation by damaged first-order sensory neurons and their peripheral axons are well-established processes that strongly contribute to pain associated with diabetic neuropathy. Studies in the past 5 years, however, suggest that, as in many neuropathic pain disorders, central neuropathic mechanisms can also contribute to pain experienced with diabetes. These studies have demonstrated that thalamic dysfunction occurs in patients with diabetes mellitus, and that in experimental models of this disease neurons in the ventral posterolateral thalamus can become hyperexcitable, firing at abnormally high frequencies and generating aberrant spontaneous activity. In this article, we discuss these findings, which suggest that thalamic neurons can act as central generators or amplifiers of pain in diabetes.
Author affiliations
T. Z. Fischer & S. G. Waxman
Yale University Center for Neuroscience and Regeneration Research, Veterans Affairs Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT 06516, USA (T. Z. Fischer, S. G. Waxman).
Correspondence to: S. G. Waxman stephen.waxman@yale.edu
Published online 13 July 2010
Nature Reviews Neurology 6, 462-466 (August 2010) | doi:10.1038/nrneurol.2010.90
Cortical lesions in multiple sclerosis
Massimiliano Calabrese, Massimo Filippi & Paolo Gallo About the authors
Abstract
Multiple sclerosis (MS) is typically considered to be a chronic inflammatory–demyelinating disease of CNS white matter. In the past decade, however, pathological and MRI studies have shown that lesions are often located in the gray matter, especially in the cerebral cortex. The histopathological characteristics of these cortical lesions differ substantially from lesions located in the white matter, which suggests location-dependent expression of the MS immunopathological process. Double inversion recovery imaging—an MRI technique that selectively images gray matter and lesions—has enabled researchers to image cortical lesions in vivo. Double inversion recovery studies have shown that cortical lesions can be detected at the earliest clinical stages of MS, and cortical lesion burden positively correlates with the severity of physical and cognitive impairments. These gray matter lesions are also independent predictors of subsequent disease evolution. This Review provides a summary of the main histopathological and MRI findings with regard to cortical lesions in MS, and indicates that increasing our understanding of cortical lesions has increased our knowledge of MS pathobiology.
Nature Reviews Neurology 6, 438-444 (August 2010) | doi:10.1038/nrneurol.2010.93
Headache: Migraine, magnetic stimulation and cortical excitability
Yew L. Lo
Abstract
Migraine is a prevalent condition that substantially reduces the quality of life of individuals who experience attacks. Numerous prescription drugs are available to treat the symptoms of migraine, but not all patients receive adequate pain relief from these over-the-counter medications.
Nature Reviews Neurology 6, 425-427 (August 2010) | doi:10.1038/nrneurol.2010.109
Alzheimer disease: Clinical use of cholinergic drugs in Alzheimer disease
Nature Reviews Neurology 6, 418-420 (August 2010) |doi:10.1038/nrneurol.2010.105
Drugs acting on the cholinergic system can improve or worsen cognitive abilities, and their effects are particularly pronounced in frail elderly individuals and patients with Alzheimer disease. Guidelines are urgently needed on the judicious use of cholinergic drugs.
Cholinesterase inhibitors remain pivotal to the treatment of Alzheimer disease (AD), but no specific guidelines are currently available regarding appropriate switching and discontinuation of these drugs. Gardette et al. sought to identify predictive factors of discontinuation and switching of cholinesterase inhibitors over a 2 year period in a multicenter cohort of community-dwelling patients with mild to moderate AD (Mini Mental State Examination score 10–26).1 Of the 686 patients enrolled, 611 were treated with cholinesterase inhibitors at baseline and scheduled for biannual follow-up. At 2 years, only 326 patients attended the fifth and final visit. Cholinesterase inhibitor switch and discontinuation incidence rates were 9.2 per 100 person-years (median time to event 10 months) and 3.6 per 100 person-years (median time to event 5 months), respectively. Ineffective cholinesterase inhibitor dose (adjusted hazard ratio [HRa] 6.91), rapid cognitive decline (HRa 4.10), hospitalization unrelated to AD (HRa 2.33) and anxiety score ≥4 on the Neuropsychiatric Inventory (HRa 2.08) were independently and significantly associated with switching to another cholinesterase inhibitor. Use of anticholinergic medication (HRa 4.26), hospitalization (AD-related: HRa 9.14, not AD-related: HRa 4.23), and weight loss (HRa 3.77) were independently and significantly associated with discontinuation of cholinesterase inhibitors.
Gardette et al. hypothesized that rapid cognitive decline was a marker for disease progression and often led to switching to another cholinesterase inhibitor in order to obtain a better response.1 Anxiety might be a predictive factor for switching because patients exhibiting anxiety related to their disease are surrounded by anxious caregivers who ask for a medication change on the patient's behalf. Alternatively, anxiety could be an adverse effect of the cholinesterase inhibitor itself or a symptom of the illness recognized by the clinician, leading them to change the patient's medications. The authors suggested that an ineffective dose of cholinesterase inhibitor could be explained by intolerance to medication, which would ultimately lead to switching.
Gardette et al. point out that weight loss is often seen with progression of AD and might, therefore, be a marker for end-stage dementia, at which stage cholinesterase inhibitors may be stopped owing to their uncertain benefits.1 The authors explain that a specialist might also choose to stop cholinesterase inhibitors when the patient is concomitantly receiving anticholinergic drugs because of awareness of the inappropriateness of the combination or perceived lack of effectiveness of the cholinesterase inhibitors. Why a specialist would choose to discontinue the cholinesterase inhibitors as opposed to the anticholinergic medications, however, is difficult to explain. Hospitalization seems to be a time where the efficacy and tolerance of cholinesterase inhibitors are reassessed, leading to switching (when the hospitalization is not AD related) or discontinuation (regardless of cause of hospitalization). Alternatively, changes in medication might reflect the internist's preference and knowledge of cholinesterase inhibitors. As suggested by Gardette et al., hospitalization for non-AD reasons can lead to stopping or changing cholinesterase inhibitors in light of a newly discovered contraindication or new drug–drug interaction.
Gardette et al.'s study has several limitations.1 Given that the patients were enrolled from AD expert centers, a selection bias might have been present. At the time of study enrollment, 531 of the patients had been on cholinesterase inhibitors for a median period of 6 months (the drugs were prescribed to the remaining 80 patients during the initial visit). The majority of the patients, therefore, had already demonstrated that they could tolerate the drugs, as most adverse effects with this type of medication are seen shortly after initiation. In addition, patients who have found the medication to be effective are more likely to continue with the treatment than are non-responders. These caveats might explain why Gardette et al.'s low discontinuation rate was incongruent with earlier persistence data obtained from pharmacy claims and randomized trial studies. Time to switch or discontinuation was calculated from the time of study inclusion and not from initiation of cholinesterase inhibitors, thereby limiting the usefulness of the resulting information. Given the high drop-out rate at 2 years, an attrition bias could also be present.
AD is conceptualized as a state of acetylcholine deficit. Cholinesterase inhibitors all inhibit the acetylcholinesterase enzyme, thereby increasing the amount of available acetylcholine. The differing pharmacodynamic and pharmacokinetic profiles of the cholinesterase inhibitors available on the market explain why these medications might have different efficacies and adverse effects in a given individual. Lack or loss of efficacy of, or intolerance to one cholinesterase inhibitor might prompt a switch to another drug in this class. The British Association for Psychopharmacology Dementia Consensus Group concluded that type 2b evidence exists to support switching to another cholinesterase inhibitor for reasons of inefficacy or intolerance.2
The question of when to discontinue cholinesterase inhibitors remains elusive. Most randomized controlled trials of cholinesterase inhibitors have lasted no longer than 6 months. Studies have, however, shown that patients can still benefit from cholinesterase inhibitors even after they have developed severe AD.3
One of the important issues raised by Gardette et al.'s study is the concomitant use of anticholinergic medications in patients receiving cholinesterase inhibitors. In this study, 6–9% of patients were receiving anticholinergic medications at one of the visits to the clinic. This figure is surprisingly high given that these patients were recruited at AD expert centers, where specialists are likely to be aware of the inappropriateness of the combination. In primary care clinics, the proportion of patients receiving both classes of medication is likely to be even higher. In a Canadian study by Herrmann et al.,4 37% of 28,961 patients treated with cholinesterase inhibitors were concomitantly receiving anticholinergic medications or benzodiazepines. In a Rhode Island Medicaid program study,5 60% of 1,183 patients taking cholinesterase inhibitors were also receiving medications known to impair cognition. These patients were less likely than the others to continue cholinesterase inhibitor therapy after 6 months. Clinicians should carefully weigh up the risks and benefits of prescribing anticholinergic medications in patients with AD. In Gardette et al.'s study, the anticholinergic drugs most often prescribed were hydroxyzine—an antihistamine prescribed for allergic reactions and sometimes for agitation or anxiety—and urinary antispasmodics.1 Cetirizine (a major metabolite of hydroxyzine) and loratadine are antihistamines that exhibit poor penetration of the blood–brain barrier and might, therefore, represent alternatives for the treatment of allergic reactions. Nontricyclic antidepressants such as selective serotonin reuptake inhibitors can be tried for the treatment of anxiety and agitation instead of hydroxyzine. To treat incontinence in patients with AD, behavioral modification or prompted voiding, rather than the use of antispasmodics, should be encouraged in the first instance. Optimizing the use of incontinence pads could be another alternative to antispasmodics. In the Gardette et al. study, 16.9% of patients were receiving benzodiazepines, but the authors do not specify whether use of these drugs was regular or sporadic. Benzodiazepines are associated with impaired cognition as well as falls and fractures in the elderly, and should be used sparingly.
In conclusion, Gardette et al.'s study sheds light on the factors that predict switching and discontinuation of cholinesterase inhibitors in mild to moderate AD. More importantly, the study illustrates the importance of developing clear guidelines for switching and discontinuing cholinesterase inhibitors and the need to familiarize clinicians with the judicious use of medications that can impair cognition.
References
-
Gardette, V. et al. Predictive factors of discontinuation and switch of cholinesterase inhibitors in community-dwelling patients with Alzheimer's disease: a 2-year prospective, multicentre, cohort study. CNS Drugs 24, 431–442 (2010).
-
Burns, A. et al. Clinical practice with anti-dementia drugs: a consensus statement from British Association for Psychopharmacology. J. Psychopharmacol. 20, 732–755 (2006).
-
Rodda, J. & Walker, Z. Ten years of cholinesterase inhibitors. Int. J. Geriatr. Psychiatry24, 437–442 (2009).
-
Herrmann, N. et al. A population-based study of cholinesterase inhibitor use for dementia. J. Am. Geriatr. Soc. 55, 1517–1523 (2007).
-
Kogut, S. J., El-Maouche, D. & Abughosh, S. M. Decreased persistence to cholinesterase inhibitor therapy with concomitant use of drugs that can impair cognition.Pharmacotherapy 25, 1729–1735 (2005).
Wednesday, August 4, 2010
Antidote for leishmaniasis
New research has identified several organic compounds that could inhibit the growth ofLeishmania parasites, known to cause leishmaniasis in humans1. Guided by a computer-aided drug design system, the research has shown that the organic compounds block the activity of an enzyme that is key to the survival of these parasites in the host.
The study may help the development of drugs against leishmaniasis, which claims around 500,000 to 1 million lives every year across the globe. Existing therapies for leishmaniasis are toxic to humans and have also resulted in the emergence of drug-resistant parasitic strains.
The researchers studied a potential drug development target trypanothione reductase (TryR), an enzyme that helps the metabolic activities of the parasite for its survival in the host. TryR has ealier been successful in drug design studies on Trypanosoma cruzi, a parasite that causes Chagas disease.
The researchers chose to target TryR of Leishmania infantum and tested the inhibitory activities of three types of trycyclic organic compounds. They found that all the compounds bind to the active site of the enzyme through the formation of hydrogen bonds. The modelled binding modes provide an insight into the interactions of these compounds with the enzyme, and thus could be used for the design and synthesis of specific inhibitors.
"Because TryR is unique in the Leishmania parasite and is not found in the mammalian host, these TryR-targeted compounds may be exploited to yield safe, affordable drugs," says lead researcher Vikash Kumar Dubey.
-
References
http://www.nature.com/nindia/2010/100728/full/nindia.2010.100.html
doi:10.1038/nindia.2010.100; Published online 28 July 2010
Sunday, August 1, 2010
Guardian of genome: Protein helps prevent damaged DNA in yeast
http://www.eurekalert.org/pub_releases/2010-08/cu-ot073010.php
Like a scout that runs ahead to spot signs of damage, a protein in yeast safeguards the yeast cell’s genome during replication.
Researchers from Cornell University’s Weill Institute for Cell and Molecular Biology have discovered how a protein called Mec1 plays the role of “guardian of the genome”, explained Marcus Smolka, assistant professor of molecular biology and genetics. The findings, “DNA Damage Signalling Recruits the Rtt 107-Six4 Scaffolds via Dpb11 to Mediate Replication Stress Response,” published in Jornal Molecualar Cell, July 30,2010.
Previous Studies have shown that cells lacking Mec1 accumulate damaged DNA and become more sensitive to agents that interfere with replication. The researchers report that the Mec1 protein monitors and repairs the machinery responsible for replicating the DNA. At times, when DNA becomes damaged, the replication machinery can actually detach from the DNA, but Mec1 coordinates the repair of the machinery and the DNA itself, allowing it to restart and continue replicating.
“Mec1 organize the cell’s response against things that jeopardize the integrity of the genome,” Smolka said.
During replication process, Mec1 accumulates at trouble spots such as lesions in the DNA or other blocks to replication. Mec1 is know as a kinase, a type of enzyme that modifies other proteins by adding a phosphate group to them, phosphorylation, which then leads to functional change in the protein. Mec1 adds a phosphate group to a protein known as Six4, which then triggers Six4 to anchor to the replication machinery. Six4 then can employ a variety of tools to repair DNA and the replication machinery.
The findings are important because researchers have discovered counterparts, orthologues to Mec1 & related proteins with similar biological pathways in humans. Also, mutations to the human genes that produce Mec1 and related proteins can lead to cancer predisposition and neurological disorders.At the same time, cancer cells employ their own similar replication repair system.
Recently, other researchers discovered that the human version of Mec1 called ATR, phosphorylates a protein that is the human counterpart to Six4. The next step, Smolka said, will be to see if after phosphorylation the human Six4 also anchors to the replication machinery to repair any damaged machinery or DNA.
Thursday, July 22, 2010
Ecology: A world without mosquitoes
Nature 466, 432-434, doi:10.1038/466432a
Eradicating any organism would have serious consequences for ecosystems- wouldn’t it? Not when it comes to mosquitoes,finds Janet Frang.
Every day, Jittawandee Murphy unlocaks a hot, padloacked room at the Walter Reed Army Institute of Research in Silver Spring, Maryland to a swarm of malaria carrying mosquitoes Anopheles stephensi. She gives million of larvae a diet of ground up fish food, and offers the gravid females blood to suck from the bellies of unconscious mice they drain 24 of the rodents a month. Murphy has been studying mosquitoes for 20 years, working on ways to limit the spread of the parasites they carry. Still, she says she would rather they were wiped off the Earth.
That sentiments is widely shared. Malaria infects some 247 million people worldwide each year, and kills nearly one million. Mosquitoes cause a huge further medical and financial burden by spreading yellow fever, dengue fever, Japaneses encephalitis, Rift Valley fever, Chikunjunya virus and West Nile virus. the there’s the pest factor: they form swarms thick enough to asphyxiate caribous in Alaska and now, as their numbers reach a seasonal peack, their probosises are plunged into human flesh across the Northern Hemisphere.
So what would happen if there were none? Would anyone or anything miss them? This question is asked to scientists who explore aspects of mosquito biology and ecology and unearthed some surprising answers.
There are 3,500 named species of mosquito of which only a couple of hundred bite or bother humans. They live on almost every continent and habitat, and serve important functions in numerous ecosystems. “Mosquitoes have been on Earth for more than 100 million years,” says Murphy, “ and they have co-evolved with so many species along the way.” Wiping out a species of mosquitoes could leave a predator without prey, or a plant without pollinator. And exploring a world without mosquitoes is more than an exercise in imagination: intense efforts are under way to develop methods that might rid the world of the most pernicious, disease carrying species.
Yet in many cases, scientists acknowledge that the ecological scar left by a missing mosquito would heal quickly as the niche was filled by other organisms. Life would continue as before or even better. When it comes to the major disease vectors, “it’s difficult to see what the downside would be to removal, except for collateral damage,” says insect ecologist Steven Juliano, of Illinois State University in Normal. A world without mosquitoes would be “more secure for us”, says medical entomologist Carlos Brisola Marcondes from the Federal University of Santa Catarina in Brazil. “The elimination of Anopheles would be very significant for mankind.”
Arctic Pests:Elimination of mosquitoes might make the biggest ecological difference in the Arctic tundra, home to mosquito species including Aedes impiger and Aedes nigripes. Eggs laid by the insects hatch the next year after snow melts, and development to adults takes only 3-4 weeks. From northern Canada to Russia, there is a brief period in which they are extraordinarily abundant, in some areas forming thick clouds. “That’s an exceptionally rare situation worldwide,” says entomologist Daniel Strickman, programme leader for medical and urban entomology at the US Department of Agriculture in Beltsville, Maryland. “There is no other place in the world where they are that much biomass.”
Views differ on what would happen if that biomass vanished. Bruce Harrison, an entomologist at the North Carolina Department of Environment and Natural Resources in Winston Salem estimates that the number of migratory birds that nest in the tundra could drop by more than 50% without mosquitoes to eat.Other researchers disagree. Cathy Curby, a wildlife biologist at the US Fish and Wildlife Services in Fairbands, Alaska, says that Arctic mosquitoes don’t show up in bird stomach samples in high numbers, and that midges are a more important source of food. “Wee as humans may overestimate the number of mosquitoes in the Arctic because they are selectively attracted to us,” She says.
Mosquitoes consume up to 300 milliliters of blood a day from each animal in a caribou heard, which are thought to select paths facing into the wind to escape the swarm. A small change in path can have major consequences in an Arctic valley through which thousands of caribou migrate, trampling the ground, eating lichens, transporting nutrients, feeding wolves and generally altering the ecology. Taken all together,then, mosquitoes would be missed in the Arctic but is the same true elsewhere?
food on the wing:”Mosquitoes are delectable things to eat and they’re easy to catch,” says aquatic entomologist Richard Merritt, at Michigan State University in East Lansing. In the absence of their larvae, hundreds of species of fish would have to change their diet to survive. “This may sound simple, but traits such as feeding behaviour are deeply imprinted, genetically, in those fish,” says Harrison. The mosquito fish Gambusia affinis for example is a specialized predator so effective at killing mosquitoes that it is stocked in rice fields and swimming pools as pest control that could go extinct. And the loss of these or other fish could have major effects up and down the food chain.
Many species of insect, spider, salamander, lizard and frog would also lose a primary food source. In one study published last month, researchers tracked insect eating house martins at a park in Camargue,France, after the area was sprayed with a microbial mosquito control agent. They found that the birds produced on average two chicks per nest after spraying, compared with three for birds at control sites.
Most mosquito eating birds would probably switch to other insects that, post mosquitoes, might emerge in large numbers to take their place. Other insectivores might not miss them at all: bats feed mostly on moths, and less than 2% of their gut content is mosquitoes. “If you’re expending energy,” says medical entomologist Janet McAllister of the Centers for Disease Control and Prevention in Fort Collins, Colorado,” are you going to eat the
Thursday, May 7, 2009
'Self-monitoring device' for HIV
- Scientists at three of London's largest research centres have been granted £2m to develop a hi-tech, finger prick blood-testing gadget.
- The device's tiny mechanical sensors - microcantilever arrays - measure HIV levels to warn of impending flare ups.
- A display then alerts the user if there is any need for them to visit a doctor.
Investigator Dr Anna-Maria Goretti, an NHS consultant and co-investigator based at the Royal Free Hospital, said: "If patients neglect to take their treatments or need prompting to see their GP the device will provide a simple way of letting them know.
-
"It will really empower HIV patients to keep a close eye on their health and their treatments."
-
Instead of routinely seeing a specialist every three or so months "just in case", they would only need to see their doctor when things were going wrong
-
As well as reducing visits to the doctor, it could also be of real benefit in developing countries where rapid and affordable ways to monitor HIV patients are urgently needed, say the researchers.
The microcantilever arrays are each coated with substances that stick to the HIV and other proteins, which are markers associated with disease progression.
Accommodating these markers causes the highly-sensitive sensors to bend like a diving board and this bend indicates the level of virus in the body, explained lead investigator Dr Rachel McKendry of University College London and the London Centre for Nanotechnology.
-
"We have used microcantilever arrays to investigate drug resistance in superbugs such as MRSA, and are excited by the opportunity to extend this approach to detecting HIV markers," she said.
-
Dr McKendry is working with Imperial College London, Cambridge Medical Innovations, Sphere Medical Ltd and BionanoConsulting on the three-year project to develop the prototype hand-held device for clinical trials.
-
Lisa Power of the Terrence Higgins Trust said: "This is certainly a very good idea. If you have diabetes you can check your blood sugar levels.
-
"Similarly, it would be very useful if HIV patients could check their own viral measures, say, once a month."
"It would not replace specialist advice, but it would be a way to reduce a patient's dependence on doctors."