what is 'chikungunya?
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While supportive or palliative medical care with anti-inflammatories and analgesics is available, there is no specific treatment for chikungunya. The illness is usually self-limiting and will resolve with time. Symptomatic treatment is recommended after excluding other more dangerous diseases.
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The Irukandji jellyfish (Carukia barnesi) is a small, extremely venomous box jellyfish. Its bada-ss, a wonder of evolutionary genetics.\n\nIts smaller then a fingernail, with very long hair thin tentacles nearly invisible in the water. Recently discovered, we know very little because it is so fragile and almost impossible to keep alive in habitation.\n\nhttp://www.youtube.com/watch?v=XPtqVh4fcoc check out the video, I do believe this woman was sick for 2-weeks. Described as an unending staircase of pain where the most potent morphine injection barely takes the edge off! Like having your spine smashed over and over again.\n\nThat woman had a dead tentacle swipe across her wrist. After getting out of the water. she was covered head to toe in a scuba outfit. She was stung while researching this animal, being aware of its potency. Imagine running into this bugger unknowingly like a normal recreational swimmer.  It is unknown how many deaths from Irukandji syndrome have been wrongly attributed to other causes.
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I thought this was an amazing article. It was just published a few days ago:\n\nWASHINGTON - Twenty-five years after the first AIDS cases emerged, scientists have confirmed that the HIV virus plaguing humans really did originate in wild chimpanzees, in a corner of Cameroon.\n\nSolving the mystery of HIV’s ancestry was dirty work. Scientists employed trackers to plunge through dense jungle and collect the fresh feces of wild apes — more than 1,300 samples in all.\n\nBefore that, it took seven years of research just to develop the testing methods to genetically trace the primate version of the virus in living wild chimps without hurting the endangered species.\n\nUntil now, “no one was able to look. No one had the tools,” said Dr. Beatrice Hahn of the University of Alabama at Birmingham. She led the team of international researchers that reported the success in Friday’s edition of the journal Science.\n\n“We’re 25 years into this pandemic,” Hahn said. “We don’t have a cure. We don’t have a vaccine. But we know where it came from. At least we can make a check mark on one of those.”\n\nScientists long have known that nonhuman primates carry their own version of the AIDS virus, called SIV or simian immunodeficiency virus. But with one exception, it had been found only in captive chimpanzees, particularly a subspecies that in the wild populates mostly West Africa.\n\nIt was not known how prevalent the virus was in chimps in the wild, or how genetically or geographically diverse it was, complicating efforts to pin down the jump from animal to man.\n\nHahn’s team tested chimp feces for SIV antibodies, finding them in a subspecies called Pan troglodytes troglodytes in southern Cameroon.\n\nChimps tend to form geographically distinct communities. By genetically analyzing the feces, researchers could trace individual infected chimps. The team found some chimp communities with infection rates as high as 35 percent, while others had no infection at all.\n\nEvery single infected chimp had a common base genetic pattern that indicated a common ancestor, Hahn said.\n\nThere are three types of HIV-1, the strain of the human virus responsible for most of the worldwide epidemic. Genetic analysis let Hahn identify chimp communities near Cameroon’s Sanaga River whose viral strains are most closely related to the most common of those HIV-1 subtypes.\n\n“The genetic similarity was striking,” Hahn said.\n\nThe first human known to be infected with HIV was a man from Kinshasa in the nearby country of Congo who had his blood stored in 1959 as part of a medical study, decades before scientists knew the AIDS virus existed.\n\nPresumably, someone in rural Cameroon was bitten by a chimp or was cut while butchering one and became infected with the ape virus. That person passed it to someone else.\n\nThe Sanaga River long has been a commercial waterway, for transporting hardwood, ivory and other items to more urban areas. Eventually, someone infected made it to Kinshasa.\n\n“How many different transmission events occurred between that initial hunter and this virus making it to Kinshasa, I don’t know. It could have been one, it could have been 10, it could have been 100,” Hahn said. “Eventually, it ended up in an urban area, and that’s where it really got going.”\n\nSomewhere in all that spread, the virus became more deadly to people than it is to chimps, who seldom are bothered much by SIV.\n\nThe research seems to settle any question of HIV’s origin, said Dr. Anthony Fauci, the National Institutes of Health’s AIDS chief.\n\nWhen tracing a virus’ evolution, “it’s important to get as close to the source as you can,” he said. “It’s of historic interest.”
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be allert of dengue\nuse mortin\nDengue fever and dengue hemorrhagic fever  are acute febrile diseases, found in the tropics, with a geographical spread similar to malaria. Caused by virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. Dengue is transmitted to humans by the mosquito Aedes aegypti (rarely Aedes albopictus).\n\nSymptoms\n\nThis infectious disease is manifested by a sudden onset of fever, with severe headache, muscle and joint pains (myalgias and arthralgias — severe pain gives it the name break-bone fever or bonecrusher disease) and rashes; the dengue rash is characteristically bright red petechia and usually appears first on the lower limbs and the chest - in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting or diarrhea.\n\nThe classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the fever (the so-called "biphasic pattern"). Clinically, the platelet count will drop until the patient's temperature is normal.\n\nCases of DHF also shows higher fever, haemorrhagic phenomena, thrombocytopenia and haemoconcentration. A small proportion of cases leads to dengue shock syndrome (DSS) which has a high mortality rate.\n\nDiagnosis\n\nThe diagnosis of dengue is usually made clinically. The classic picture is high fever with no localising source of infection, a petechial rash with thrombocytopenia and relative leukopenia.\n\nThere exists a WHO definition of dengue haemorrhagic fever that has been in use since 1975; all four criteria must be fulfilled:\n\n1. Fever\n2. Haemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)\n3. Thrombocytopaenia (<100 platelets per mm³ or estimated as less than 3 platelets per high power field)\n4. Evidence of plasma leakage (hematocrit more than 20% higher than expected, or drop in haematocrit of 20% or more from baseline following IV fluid, pleural effusion, ascites, hypoproteinaemia)\n\nDengue shock syndrome is defined as dengue haemorrhagic fever plus:\n\n# Weak rapid pulse,\n# Narrow pulse pressure (less than 20 mm Hg)\n\n# Hypotension for age;\n#Cold, clammy skin and restlessness.\n\nSerology and PCR (polymerase chain reaction) studies are available to confirm the diagnosis of dengue if clinically indicated.\n\nTreatment\n\nThe mainstay of treatment is supportive therapy. The patient is encouraged to keep up oral intake, especially of oral fluids. If the patient is unable to maintain oral intake, supplementation with intravenous fluids may be necessary to prevent dehydration and significant hemoconcentration. A platelet transfusion is rarely indicated if the platelet level drops significantly or if there is significant bleeding. But the transfusion is recommendable on platelet count falling below 20,000 without hemorrhage / bleeding or approx 50,000 with hemorrhage/bleeding. Internal bleeding indicated by dark color of stools, other bleedings indicated at surface as red rashes all over or most of the body parts.
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Treatment\n\nChikungunya fever is not a life threatening infection. Symptomatic treatment for mitigating pain and fever using anti-inflammatory drugs along with rest usually suffices. While recovery from chikungunya is the expected outcome, convalescence can be prolonged (up to a year or more), and persistent joint pain may require analgesic (pain medication) and long-term anti-inflammatory therapy. \n\nPrevention and control\n\nNo vaccine is available against this virus infection. Prevention is entirely dependent upon taking steps to avoid mosquito bites and elimination of mosquito breeding sites. \n\nTo avoid mosquito bites:\n\n     Wear full sleeve clothes and long dresses to cover the limbs;\n\n     Use mosquito coils, repellents and electric vapour mats during the daytime;\n\n     Use mosquito nets – to protect babies, old people and others, who may rest during the day. The effectiveness of such nets can be improved by treating them with permethrin (pyrethroid insecticide). Curtains (cloth or bamboo) can also be treated with insecticide and hung at windows or doorways, to repel or kill mosquitoes.\n\n     Mosquitoes become infected when they bite people who are sick with chikungunya. Mosquito nets and mosquito nets and mosquito coils will effectively prevent mosquitoes from biting sick people.\n\nTo prevent mosquito breeding\n\nThe Aedes mosquitoes that transmit chikungunya breed in a wide variety of manmade containers which are common around human dwellings. These containers collect rainwater, and include discarded tires, flowerpots, old oil drums, animal water troughs, water storage vessels, and plastic food containers. These breeding sites can be eliminated by\n\n      Draining water from coolers, tanks, barrels, drums and buckets, etc.;\n\n      Emptying coolers when not in use;\n\n      Removing from the house all objects, e.g. plant saucers, etc. which have water collected in them\n\n      Cooperating with the public health authorities in anti-mosquito measures.\n\n\n\nreff:http://www.searo.who.int/en/Section10/Section2246.htm
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WHO is the specialized organizaton of UN. They are for sure trying to eradicate this virus. that is their area of work anyway.
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First check the symptoms your brother has.\n\nThe common symptoms of chikungunya include fever which can reach 39 °C, (102.2 °F) a petechial or maculopapular rash usually involving the limbs and trunk, and arthralgia or arthritis affecting multiple joints which can be debilitating. There can also be headache, conjunctival injection and slight photophobia.\n\nAs for the treatment:\n\nWhile supportive or palliative medical care with anti-inflammatories and analgesics is available, there is no specific treatment for chikungunya. The illness is usually self-limiting and will resolve with time. Symptomatic treatment is recommended after excluding other more dangerous diseases. Vaccine trials were carried out in 2000, but funding for the project was discontinued and there is no vaccine currently available.\n\nA serological test for chikungunya is available from the University of Malaya in Kuala Lumpur, Malaysia.\n\nPossible role for chloroquine in the treatment of chikungunya: There is an interesting dialogue, mostly in French, about the possible use of chloroquine in the treatment of the arthralgia associated with CHIK.\n\n1. A paper published in South Africa in 1984 concerning 10 cases of CHIK showed some effect of CQ in treating the symptoms of arthritis. Brighton SW. Chloroquine phosphate treatment of chronic Chikungunya arthritis. An open pilot study. S Afr Med J 1984 Aug 11;66(6):217-8.\n\nThe abstract of the paper: "Over 12% of patients who contract Chikungunya virus infection develop chronic joint symptoms. These symptoms respond only partially to the non-steroidal anti-inflammatory drugs. An open pilot study on the efficacy of chloroquine phosphate was carried out and 10 patients completed 20 weeks of therapy. Both the Ritchie articular index and morning stiffness improved significantly. In the patient's assessment, 7 out of 10 considered their conditions to have improved. On the basis of the doctor's assessment, 5 of the 10 had improved. These results justify further controlled blind trials of chloroquine in chronic Chikungunya arthritis."\n\n2. From the University of Malaya: http://www.vadscorner.com/alphaviruses.html\n\n"Treatment [of chikungunya]:\n\nSupportive care with rest is indicated during the acute joint symptoms. Movement and mild exercise tend to improve stiffness and morning arthralgia, but heavy exercise may exacerbate rheumatic symptoms. In unresolved arthritis refractory to aspirin and nonsteroidal antiinflammatory drugs, chloroquine phosphate (250 mg/day) has given promising results."\n\n3. From the French government (in French): http://agmed.sante.gouv.fr/pdf/10/chicungu.pdf\n\n"Dans le cadre de l'enquête mise en place pour identifier les molécules actives contre le virus du Chikungunya, des essais ont été réalisés en laboratoire sur des cultures cellulaires in vitro et ont montré une activité antivirale de la chloroquine (Nivaquine®) sur ce virus. L'Agence française de sécurité sanitaire des produits de santé (Afssaps) relève qu'il s'agit de tests préliminaires et qu'à ce stade, aucune donnée d'efficacité et de sécurité n'est disponible chez l'homme.\n\nDans ce contexte, l'Agence rappelle les indications et les conditions d'un bon usage de la Nivaquine®. La Nivaquine® est indiquée principalement dans le traitement préventif et curatif du paludisme. Elle aussi utilisée dans le traitement des symptômes de la polyarthrite rhumatoïde et dans le traitement du lupus. L'utilisation de ce médicament nécessite une prescription médicale."\n\nRough translation: "In the context of the search for molecules with activity against the chikungunya virus, lab tests on cell cultures in vitro have shown that chloroquine (NivaquineR) has some antiviral activity against this virus. The Fench agency of health and medicines safety (AFSSAPS) points out that this involves preliminary tests and that at this stage,
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Not a joke - it's called rabies virus.  It is an RNA rhabdovirus belonging to the order Mononegavirales, genus Lyssavirus.
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Its virus and spread from infection with unsafe sex and infected blood exchange/ transmission from infected person.
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That is probably not a trypanosomiasis. Ever been to Africa recently?
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Dengue Virus\nThe dengue virus belongs to the Family Flaviviridae. It is an enveloped plus-strand RNA arbovirus. Being an enveloped virus, it has pieces of host cell’s plasma membrane that virion acquires as it emerges from its host cell and with spikes or protruding proteins. As a plus-strand RNA virus, it is translated directly by the host ribosome.  \n\nVirus Life Cycle\nAll viruses undergo the same life cycle. First, it attaches itself to the host cell known as adsorption. Then, the genome enters the host cell in the penetration process. During the uncoating, the virus removes its capsid and envelope. It is followed by the viral synthesis wherein the host cell manufactures viral components. Then maturation process takes place as the components assembles into intact new virions. Lastly, the virus particles leaves infected cell. \n\n\nPathophysiology\nThe transmission cycle of dengue virus by the mosquito Aedes aegypti begins with a dengue-infected person. This person will have virus circulating in the blood—a viremia that lasts for about five days. During the viremic period, an uninfected female Aedes aegypti mosquito bites the person and ingests blood that contains dengue virus. Although there is some evidence of transovarial transmission of dengue virus in Aedes aegypti, usually mosquitoes are only infected by biting a viremic person.\nThen, within the mosquito, the virus replicates during an extrinsic incubation period of eight to twelve days.\nThe mosquito then bites a susceptible person and transmits the virus to him or her, as well as to every other susceptible person the mosquito bites for the rest of its lifetime.\nThe virus then replicates in the second person and produces symptoms. The symptoms begin to appear an average of four to seven days after the mosquito bite—this is the intrinsic incubation period, within humans. While the intrinsic incubation period averages from four to seven days, it can range from three to 14 days.\nThe viremia begins slightly before the onset of symptoms. Symptoms caused by dengue infection may last three to 10 days, with an average of five days, after the onset of symptoms—so the illness persists several days after the viremia has ended.\nTransmission cycle that takes place within the human body.\n1.The virus is inoculated into humans with the mosquito saliva.\n2.The virus localizes and replicates in various target organs, for example, local lymph nodes and the liver.\n3.The virus is then released from these tissues and spreads through the blood to infect white blood cells and other lymphatic tissues.\n4.The virus is then released from these tissues and circulates in the blood.\nTransmission cycle that takes place within the mosquito.\n5.The mosquito ingests blood containing the virus. \n6.The virus replicates in the mosquito midgut, the ovaries, nerve tissue and fat body. It then escapes into the body cavity, and later infects the salivary glands. \n7.The virus replicates in the salivary glands and when the mosquito bites another human, the cycle continues.\nThere are 4 Serotypes of Dengue virus (1,2,3,4 Group B arbovirus). The first attack, neutralizing antibodies are produced principally against this virus type inoculated by the mosquito vector.  Although antigenetically linked to each other, they may only give partial cross-protection, after being infected by any of them. \nThe pathogenesis of hemorrhagic dengue fever is the result of many factors. As the dengue virus attacks the human body, the immune complex or antibody tries to fight off the virus resulting to anaphylactic reactions that produce toxic substances such as histamine, serotonins, and bradyknin which damage the capillary walls. These are responsible for the increase in vascular permeability exhibiting symptoms such as macopopular, rashes, pruritus, edematous extremities, and flushed skin.  Increase in vascular permeability causes extravasation of fluids resulting to fluid shifts especially in the abdomen, p
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DICLOFENAC SODIUM  is an NON STEROIDAL ANTI INFLAMMATORY DRUG- abbreviated as NSAID.\nit causes relief of intense pain and fever of chikun gunya.\nalways take it after food or it will cause gastritis
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The Aedes aegypti, a kind of mosquito that carries both dengue and yellow fever.  There are others of the same species, such as Aedes albopictus that carries Eastern Equine Encephalitis.
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This disease is caused by mosquitoe...The disease starts with fever and severe pain in joints..the fever will subside in 3 or 4 days but the joints pain will be there for over a month...this disease is not fatal.. ............................\neverthing said in above answer is true but what i been told is that the fever stay for even longer time and currently its on the roll in many districts of KARNATKA. according to newspapers it has reached to BANGALORE district villages.
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Chikunguya is a vector-borne disease carried by Aedes mosquito, same vector that mainly causes dengue fever, very vastly affecting the tropical country like in Malaysia, Brazil etc... It really much resembles dengue fever in terms of symptoms. While dengue fever is caused by parasites (Plasmodium), Chikungunya is caused by chikunguya virus. symptoms include fever, joint pain, muscle pain and headache and some severe cases might have haemorrhagic.
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A parasitic disease.  See the attached link.
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Among the more commonly known human diseases caused by arboviridae are:\nYellow Fever (NOT Malaria)\nDengue fever\nWest Nile disease\nseveral kinds of encephalitis.