- Only the female aedes mosquito bites as it needs the protein in blood to develop its eggs.
- The mosquito becomes infective approximately 7 days after it has bitten a person carrying the virus. This is the extrinsic incubation period, during which time the virus replicates in the mosquito and reaches the salivary glands.
- Peak biting is at dawn and dusk.
- The average lifespan of an Aedes mosquito in Nature is 2 weeks
- The mosquito can lay eggs about 3 times in its lifetime, and about 100 eggs are produced each time.
- The eggs can lie dormant in dry conditions for up to about 9 months, after which they can hatch if exposed to favourable conditions, i.e. water and food
Wednesday, May 21, 2008
facts for dengue
Fast facts about the mosquito
Tuesday, May 20, 2008
Dengue
The mosquito is a disease carrier and an irritant, but the mosquito is not impossible to control. Understanding mosquitoes biology and the mosquito breeding cycle can result in effective pest control for mosquito infestiation. This pesky mosquito is found worldwide. The mosquito affects humans only in their adult stage, all other mosquitoes stages occur in water. There are about three thousand species of mosquitoes worldwide, approximately 170 species in North America. Breeding sites, biting preferences, time of day they bite and ability to transmit diseases vary with the species.Mosquitoes undergo complete metamorphosis, egg, larvae (top left,) pupae (center) and adult (bottom) The adult male feeds on nectar and is important only for mating. The female usually must have a blood feast in order to produce viable eggs and that is where the problems begin. They feed on mammals, and humans are among some species favorites. This is annoying and at times unbearable, but not as scary as the diseases some are able to carry. Certain female mosquitoes are capable of being vectors (disease carriers,) of Malaria, West Nile Virus, Yellow Fever, Dengue, and Dog Heartworm.
Breeding occurs with mosquitoes in any area there is standing water such as stagnant ponds, discarded tires, tree stumps, etc. The more rainfall per season, the more numerous the mosquitoes. With mild winters and excessive rainfalls the possibility of a troublesome mosquito season is more likely.Complete development from egg to adult varies with species and temperature, but usually takes from 10-14 days. Once the eggs hatch into larvae or wigglers they begin feeding on algae and other organic matter in the water. The larvae develop through four molts and pupate. The pupae do not feed but are mobile spending much of their time near the water surface to breathe, and after one to three days emerge as an adult. The adults mate 24-48 hours after emergence.
The male dies after six or seven days, the female, depending on the species, lives from two weeks to 3 months during the summer. Once she has had a blood meal she will lay her first and largest brood of 50-500 eggs. Subsequent broods will be smaller but there will be 8-10 broods.Consider an average brood of 200 eggs per brood and that this insect can complete its development in less than two weeks, we can obtain in only five generations some 20 million of these pests. For mosquito control. For mosquito products.
Breeding occurs with mosquitoes in any area there is standing water such as stagnant ponds, discarded tires, tree stumps, etc. The more rainfall per season, the more numerous the mosquitoes. With mild winters and excessive rainfalls the possibility of a troublesome mosquito season is more likely.Complete development from egg to adult varies with species and temperature, but usually takes from 10-14 days. Once the eggs hatch into larvae or wigglers they begin feeding on algae and other organic matter in the water. The larvae develop through four molts and pupate. The pupae do not feed but are mobile spending much of their time near the water surface to breathe, and after one to three days emerge as an adult. The adults mate 24-48 hours after emergence.
The male dies after six or seven days, the female, depending on the species, lives from two weeks to 3 months during the summer. Once she has had a blood meal she will lay her first and largest brood of 50-500 eggs. Subsequent broods will be smaller but there will be 8-10 broods.Consider an average brood of 200 eggs per brood and that this insect can complete its development in less than two weeks, we can obtain in only five generations some 20 million of these pests. For mosquito control. For mosquito products.
Monday, May 19, 2008
Dengue Fever
Dengue Fever and Dengue Haemorrhagic Fever (a more severe form) are the most common mosquito-borne viral diseases in the world.
Dengue Fever is an illness caused by infection with a virus transmitted by the Aedes mosquito. There are four types of this virus (serotypes 1 to 4) which can infect you.
Dengue Fever is spread though the bite of the Aedes MosquitoThis 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 petechiae 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.
Other symptoms include:
• fever;
• bladder problems;
• constant headaches;
• severe dizziness; and,
• loss of appetite.
best regards
不测了俄
Dengue Fever is an illness caused by infection with a virus transmitted by the Aedes mosquito. There are four types of this virus (serotypes 1 to 4) which can infect you.
Dengue Fever is spread though the bite of the Aedes MosquitoThis 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 petechiae 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.
Other symptoms include:
• fever;
• bladder problems;
• constant headaches;
• severe dizziness; and,
• loss of appetite.
best regards
不测了俄
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Beware of Mosquito
Head - This is where all the sensors are, along with the biting apparatus. The head has two compound eyes, antennae to sense chemicals and the mouth parts called the palpus and the proboscis (only females have the proboscis, for biting).
Thorax - This segment is where the two wings and six legs attach. It contains the flight muscles, compound heart, some nerve cell ganglia and trachioles.
Abdomen - This segment contains the digestive and excretory
organs.
Thorax - This segment is where the two wings and six legs attach. It contains the flight muscles, compound heart, some nerve cell ganglia and trachioles.
Abdomen - This segment contains the digestive and excretory
organs.
This are the places that mosquito will breed. We must be fast before they breed and we bleed.
Mosquito-borne-diseases
don't be dirty fellow like bruce lee taking martial arts to protect himself from school bullies
MALARIA
Malaria is bruce lee taking martial arts to protect himself from school bullies vector-borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americas, Asia, and Africa. Each year, there are approximately 515 million cases of malaria, killing between one and three million people, the majority of whom are young children in Sub-Saharan Africa.[1] Malaria is commonly associated with poverty, but is also a cause of poverty and a major hindrance to economic development.
Malaria is one of the most common infectious diseases and an enormous public health problem. The disease is caused by protozoan parasites of the genus Plasmodium. Only four types of the plasmodium parasite can infect humans; the most serious forms of the disease are caused by Plasmodium falciparum and Plasmodium vivax, but other related species (Plasmodium ovale, Plasmodium malariae) can also affect humans. This group of human-pathogenic Plasmodium species is usually referred to as malaria parasites.
Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (light headedness, shortness of breath, tachycardia etc.), as well as other general symptoms such as fever, chills, nausea, flu-like illness, and in severe cases, coma and death. Malaria transmission can be reduced by preventing mosquito bites with mosquito nets and insect repellents, or by mosquito control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs.
DENGUE FEVER
"Dengue Fever" redirects here. For the band of the same name, see Dengue fever (IPA: /ˈdɛŋgeɪ/) and dengue hemorrhagic fever (DHF) are acute febrile diseases, found in the tropics and Africa, and caused by four closely related virus serotypes of the genus Flavivirus, family Flaviviridae.[1] The geographical spread is similar to malaria, but unlike malaria, dengue is often found in urban areas of tropical nations, including Singapore, Taiwan, Indonesia, Philippines, India and Brazil. 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 Aedes aegypti (rarely Aedes albopictus) mosquito, which feeds during the day.[2]
MALARIA
Malaria is bruce lee taking martial arts to protect himself from school bullies vector-borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americas, Asia, and Africa. Each year, there are approximately 515 million cases of malaria, killing between one and three million people, the majority of whom are young children in Sub-Saharan Africa.[1] Malaria is commonly associated with poverty, but is also a cause of poverty and a major hindrance to economic development.
Malaria is one of the most common infectious diseases and an enormous public health problem. The disease is caused by protozoan parasites of the genus Plasmodium. Only four types of the plasmodium parasite can infect humans; the most serious forms of the disease are caused by Plasmodium falciparum and Plasmodium vivax, but other related species (Plasmodium ovale, Plasmodium malariae) can also affect humans. This group of human-pathogenic Plasmodium species is usually referred to as malaria parasites.
Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (light headedness, shortness of breath, tachycardia etc.), as well as other general symptoms such as fever, chills, nausea, flu-like illness, and in severe cases, coma and death. Malaria transmission can be reduced by preventing mosquito bites with mosquito nets and insect repellents, or by mosquito control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs.
DENGUE FEVER
"Dengue Fever" redirects here. For the band of the same name, see Dengue fever (IPA: /ˈdɛŋgeɪ/) and dengue hemorrhagic fever (DHF) are acute febrile diseases, found in the tropics and Africa, and caused by four closely related virus serotypes of the genus Flavivirus, family Flaviviridae.[1] The geographical spread is similar to malaria, but unlike malaria, dengue is often found in urban areas of tropical nations, including Singapore, Taiwan, Indonesia, Philippines, India and Brazil. 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 Aedes aegypti (rarely Aedes albopictus) mosquito, which feeds during the day.[2]
PATHOGENESIS
Yellow Fever is caused by an arbovirus of the family Flaviviridae, a gram-positive single-stranded RNA virus. Human infection begins after deposition of viral particles through the skin in infected arthropod saliva. The mosquitos involved are Aedes simpsaloni, A. africanus, and A. aegypti in Africa, the Haemagogus genus in South America,[5] and the Sabethes genus in France. Yellow fever is frequently severe but moderate cases may occur as the result of previous infection by another flavivirus. After infection the virus first replicates locally, followed by transportation to the rest of the body via the lymphatic system.[6] Following systemic lymphatic infection the virus proceeds to establish itself throughout organ systems, including the heart, kidneys, adrenal glands, and the parenchyma of the liver; high viral loads are also present in the blood.[1] Necrotic masses (Councilman bodies) appear in the cytoplasm of hepatocytes.[6],[7]
Yellow fever begins suddenly after an incubation period of three to five days in the human body. In mild cases only fever and headache may be present. The severe form of the disease commences with fever, chills, bleeding into the skin, rapid heartbeat, headache, back pains, and extreme prostration. Nausea, vomiting, and constipation are common. Jaundice usually appears on the second or third day. After the third day the symptoms recede, only to return with increased severity in the final stage, during which there is a marked tendency to hemorrhage internally; the characteristic “coffee ground” vomits contains blood. The patient then lapses into delirium and coma, often followed by death. During epidemics the fatality rate was often as high as 85%. Although the disease still occurs, it is usually confined to sporadic outbreaks.
Yellow fever begins suddenly after an incubation period of three to five days in the human body. In mild cases only fever and headache may be present. The severe form of the disease commences with fever, chills, bleeding into the skin, rapid heartbeat, headache, back pains, and extreme prostration. Nausea, vomiting, and constipation are common. Jaundice usually appears on the second or third day. After the third day the symptoms recede, only to return with increased severity in the final stage, during which there is a marked tendency to hemorrhage internally; the characteristic “coffee ground” vomits contains blood. The patient then lapses into delirium and coma, often followed by death. During epidemics the fatality rate was often as high as 85%. Although the disease still occurs, it is usually confined to sporadic outbreaks.
La Crosse encephalitis
La Crosse encephalitis is an encephalitis caused by an arbovirus (the La Crosse virus) which has a mosquito vector (Aedes triseriatus). It occurs in the Appalachian and Midwestern regions of the United States. Recently there has been an increase of cases in the South East of the United States. An explanation to this may be that the mosquito Aedes albopictus is also an efficient vector of La Crosse virus. Aedes albopictus is a species that has entered the US and spread across the SE of the US and replaced Aedes aegypti in most areas (which is not an efficient vector of LAC).
La Crosse (LAC) encephalitis was discovered in La Crosse, Wisconsin in 1963. Since then, the virus has been identified in several Midwestern and Mid-Atlantic states. During an average year, about 75 cases of LAC encephalitis are reported to the CDC. Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a Bunyavirus and is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, Aedes triseriatus, and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans.
Historically, most cases of LAC encephalitis occur in the upper Midwestern states (Minnesota, Wisconsin, Iowa, Illinois, Indiana, and Ohio). Recently, more cases are being reported from states in the mid-Atlantic (West Virginia, Virginia and North Carolina) and southeastern (Alabama and Mississippi) regions of the country. It has long been suspected that LAC encephalitis has a broader distribution and a higher incidence in the eastern United States, but is under-reported because the etiologic agent is often not specifically identified.
La Crosse (LAC) encephalitis was discovered in La Crosse, Wisconsin in 1963. Since then, the virus has been identified in several Midwestern and Mid-Atlantic states. During an average year, about 75 cases of LAC encephalitis are reported to the CDC. Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a Bunyavirus and is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, Aedes triseriatus, and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans.
Historically, most cases of LAC encephalitis occur in the upper Midwestern states (Minnesota, Wisconsin, Iowa, Illinois, Indiana, and Ohio). Recently, more cases are being reported from states in the mid-Atlantic (West Virginia, Virginia and North Carolina) and southeastern (Alabama and Mississippi) regions of the country. It has long been suspected that LAC encephalitis has a broader distribution and a higher incidence in the eastern United States, but is under-reported because the etiologic agent is often not specifically identified.
Chikungunya
Chikungunya virus (CHIKV) is an arbovirus, of the genus, Alphavirus, that is transmitted to humans by virus-carrying Aedes mosquitoes.[1] There have been recent outbreaks of CHIKV associated with severe morbidity. CHIKV causes an illness with symptoms similar to dengue fever. CHIKV manifests itself with a prolonged arthralgic disease that affects the joints of the extremities. The acute febrile phase of the illness lasts only two to five days. The pain associated with CHIKV infection of the joints persists for weeks or months.[2]
Murray Valley encephalitis virus
Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis (previously known as Australian encephalitis) and in humans can cause permanent neurological disease or death. MVEV is related to Kunjin virus which has a similar ecology but has a lower morbidity rate.
MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the Ciconiiformes order, including herons and cormorants, provide the natural reservoir for MVEV[1]. The major mosquito vector is Culex annulirostris. Human infection occurs only through bites from infected mosquitoes, it cannot be transmitted from person to person [1].
The first epidemics of MVE occurred in 1917 and 1918 in Southeastern Australia following years of high rainfall. The virus was isolated from human samples in 1951 during an epidemic in the Murray Valley, Australia[2]. Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas [2]
The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease. The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have life-long immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season (November to July), when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum [3].
The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus (Hurrelbrink et al., 1999) [4]. Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection.
MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the Ciconiiformes order, including herons and cormorants, provide the natural reservoir for MVEV[1]. The major mosquito vector is Culex annulirostris. Human infection occurs only through bites from infected mosquitoes, it cannot be transmitted from person to person [1].
The first epidemics of MVE occurred in 1917 and 1918 in Southeastern Australia following years of high rainfall. The virus was isolated from human samples in 1951 during an epidemic in the Murray Valley, Australia[2]. Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas [2]
The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease. The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have life-long immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season (November to July), when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum [3].
The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus (Hurrelbrink et al., 1999) [4]. Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection.
West Nile virus
West Nile virus (or WNV) is a virus of the family Flaviviridae; part of the Japanese encephalitis (JE) antigenic complex of viruses, it is found in both tropical and temperate regions. It mainly infects birds, but is known to infect humans, horses, dogs, cats, bats, chipmunks, skunks, squirrels, and domestic rabbits. The main route of human infection is through the bite of an infected mosquito.
Image reconstructions and cryoelectron microscopy reveal a 45-50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus flavivirus within the family Flaviviridae. WNV is a positive-sense, single strand of RNA, it is between 11,000 and 12,000 nucleotides long which encode seven non-structural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12 kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins.
Japanese Encephalitis
Image reconstructions and cryoelectron microscopy reveal a 45-50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus flavivirus within the family Flaviviridae. WNV is a positive-sense, single strand of RNA, it is between 11,000 and 12,000 nucleotides long which encode seven non-structural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12 kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins.
Japanese Encephalitis
Japanese encephalitis (Japanese: 日本脳炎, Nihon-nōen; previously known as Japanese B encephalitis to distinguish it from von Economo's A encephalitis) is a disease caused by the mosquito-borne Japanese encephalitis virus. The Japanese encephalitis virus is a virus from the family Flaviviridae. Domestic pigs and wild birds are reservoirs of the virus; transmission to humans may cause severe symptoms. One of the most important vectors of this disease is the mosquito Culex tritaeniorhynchus. This disease is most prevalent in Southeast Asia and the Far East
Ross River virus
Ross River virus (RRV) is an arbovirus of the genus Alphavirus. In humans, it is the cause of an 'epidemic polyarthritis' commonly known as Ross River fever, that in Australia infected an average of about 4,000 people annually in the decade 1995-2004.[1] Ross River fever is a notifiable disease in Australia (see List of notifiable diseases#Australia).
Ross River virus is endemic to parts of Australia and Papua New Guinea, and was observed in an outbreak in the South Pacific during 1979-1980. It was named following the isolation of an arbovirus from mosquitoes trapped beside Ross River, near Townsville, Queensland, in 1959, and the subsequent identification of this virus as the one responsible for cases of epidemic polyarthritis in Queensland and New South Wales. Outbreaks as long ago as 1928 are now attributed to Ross River virus.[2][3]
Ross River fever is also known as Ross River virus infection or Ross River virus disease, since not all patients experience symptoms of fever. A review of a number of studies concluded that between 20% and 60% of patients experience fever. Similarly, the name epidemic polyarthritis fell out of use because arthritic symptoms are not observed in all patients; the same review found that between 83% and 98% of patients experienced joint pain. Other symptoms include rash. Although there is some (mostly) anecdotal evidence of long-term chronic effects due to Ross River virus, particularly joint pain, patients can typically expect to recover within a month after the onset of symptoms.[3]
In rural and regional areas of Australia, the continued prevalence of Ross River virus is thought to be supported by 'reservoir' hosts such as large marsupial mammals, but antibodies to Ross River virus have been found in a wide variety of placental and marsupial mammals, and also in a number of bird species. It is not presently known what reservoir hosts support Ross River virus in metropolitan areas such as Brisbane.[3]
The Southern Saltmarsh mosquito (Aedes camptorhyncus) which is known to carry the Ross River virus was discovered in New Zealand in 1998, and there is an ongoing eradication program by the New Zealand Ministry of Health, involving spraying the insectide Bti on infested areas. As of June 2007 there have been no reported cases of Ross River Virus that arose in New Zealand.
The study of RRV induced disease in the laboratory has been recently facilited by a mouse model. Inbred mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice, similar to humans, is characterized by an inflammatory infiltrate including macrophages which are immunopathlogic and excaberate disease. Furthermore, recent data indicate that the serum component, C3, directly contributes to disease since mice deficient in the C3 protein do not suffer from severe disease following infection.[4] Taken together, this indicates that an aberrant innate immune response is responsible for severe disease
Ross River virus is endemic to parts of Australia and Papua New Guinea, and was observed in an outbreak in the South Pacific during 1979-1980. It was named following the isolation of an arbovirus from mosquitoes trapped beside Ross River, near Townsville, Queensland, in 1959, and the subsequent identification of this virus as the one responsible for cases of epidemic polyarthritis in Queensland and New South Wales. Outbreaks as long ago as 1928 are now attributed to Ross River virus.[2][3]
Ross River fever is also known as Ross River virus infection or Ross River virus disease, since not all patients experience symptoms of fever. A review of a number of studies concluded that between 20% and 60% of patients experience fever. Similarly, the name epidemic polyarthritis fell out of use because arthritic symptoms are not observed in all patients; the same review found that between 83% and 98% of patients experienced joint pain. Other symptoms include rash. Although there is some (mostly) anecdotal evidence of long-term chronic effects due to Ross River virus, particularly joint pain, patients can typically expect to recover within a month after the onset of symptoms.[3]
In rural and regional areas of Australia, the continued prevalence of Ross River virus is thought to be supported by 'reservoir' hosts such as large marsupial mammals, but antibodies to Ross River virus have been found in a wide variety of placental and marsupial mammals, and also in a number of bird species. It is not presently known what reservoir hosts support Ross River virus in metropolitan areas such as Brisbane.[3]
The Southern Saltmarsh mosquito (Aedes camptorhyncus) which is known to carry the Ross River virus was discovered in New Zealand in 1998, and there is an ongoing eradication program by the New Zealand Ministry of Health, involving spraying the insectide Bti on infested areas. As of June 2007 there have been no reported cases of Ross River Virus that arose in New Zealand.
The study of RRV induced disease in the laboratory has been recently facilited by a mouse model. Inbred mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice, similar to humans, is characterized by an inflammatory infiltrate including macrophages which are immunopathlogic and excaberate disease. Furthermore, recent data indicate that the serum component, C3, directly contributes to disease since mice deficient in the C3 protein do not suffer from severe disease following infection.[4] Taken together, this indicates that an aberrant innate immune response is responsible for severe disease
Rift Valley fever
Rift Valley Fever (RVF) is a viral zoonosis (affects primarily domestic livestock, but can be passed to humans) causing fever. It is spread by the bite of infected mosquitoes. The disease is caused by the RVF virus, a member of the genus Phlebovirus (family Bunyaviridae). The disease was first reported among livestock in Kenya around 1915, but the virus was not isolated until 1931. RVF outbreaks occur across sub-Saharan Africa, with outbreaks occurring elsewhere infrequently (but sometimes severely - in Egypt in 1977-78, several million people were infected and thousands died during a violent epidemic. In Kenya in 1998, the virus claimed the lives of over 400 Kenyans. In September 2000 an outbreak was confirmed in Saudi Arabia and Yemen).
In humans the virus can cause several different syndromes. Usually sufferers have either no symptoms or only a mild illness with fever, headache, myalgia and liver abnormalities. In a small percentage of cases (< title="Hemorrhagic fever"> syndrome, meningoencephalitis (inflammation of the brain), or affecting the eye. Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, patients recover within 2-7 days after onset.
Distribution of Rift Valley Fever in Africa. Blue, countries with endemic disease and substantial outbreaks of RVF; green, countries known to have some cases, periodic isolation of virus, or serologic evidence of RVF.
Approximately 1% of human sufferers die of the disease. Amongst livestock the fatality level is significantly higher. In pregnant livestock infected with RVF there is the abortion of virtually 100% of fetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.
In humans the virus can cause several different syndromes. Usually sufferers have either no symptoms or only a mild illness with fever, headache, myalgia and liver abnormalities. In a small percentage of cases (< title="Hemorrhagic fever"> syndrome, meningoencephalitis (inflammation of the brain), or affecting the eye. Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, patients recover within 2-7 days after onset.
Distribution of Rift Valley Fever in Africa. Blue, countries with endemic disease and substantial outbreaks of RVF; green, countries known to have some cases, periodic isolation of virus, or serologic evidence of RVF.
Approximately 1% of human sufferers die of the disease. Amongst livestock the fatality level is significantly higher. In pregnant livestock infected with RVF there is the abortion of virtually 100% of fetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.
St. Louis Encephalitis
St. Louis Encephalitis is a disease caused by the mosquito borne St. Louis Encephalitis virus. St. Louis encephalitis virus is related to Japanese encephalitis virus. This disease mainly affects the United States. Occasional cases have been reported from Canada and Mexico.The name of the virus goes back to 1933 when within five weeks in autumn an encephalitis epidemic of explosive proportions broke out in the vicinity of St. Louis, Missouri and the neighboring St. Louis County.[1] Over 1,000 cases were reported to the local health departments and the newly constituted National Institute of Health was appealed to for epidemiological and investigative expertise. The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice. [2]
Mosquitoes, from the genus Culex, become infected by feeding on birds infected with the St. Louis encephalitis virus. Infected mosquitoes then transmit the St. Louis encephalitis virus to humans and animals during the feeding process. The St. Louis encephalitis virus grows both in the infected mosquito and the infected bird, but does not make either one sick. Only infected mosquitoes can transmit St. Louis encephalitis virus. Once a human has been infected with the virus it is not transmissible from that individual to other humans.
The majority of infections result in mild illness, including fever and headache. When infection is more severe the person may experience headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Fatality ranges from 3-30%, aged people are more likely to have a fatal infection.
There is no vaccine or any other treatments specifically for St. Louis encephalitis virus.
Mosquitoes, from the genus Culex, become infected by feeding on birds infected with the St. Louis encephalitis virus. Infected mosquitoes then transmit the St. Louis encephalitis virus to humans and animals during the feeding process. The St. Louis encephalitis virus grows both in the infected mosquito and the infected bird, but does not make either one sick. Only infected mosquitoes can transmit St. Louis encephalitis virus. Once a human has been infected with the virus it is not transmissible from that individual to other humans.
The majority of infections result in mild illness, including fever and headache. When infection is more severe the person may experience headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Fatality ranges from 3-30%, aged people are more likely to have a fatal infection.
There is no vaccine or any other treatments specifically for St. Louis encephalitis virus.
O'nyong'nyong virus
The O'nyong'nyong virus or O'nyong-nyong virus was a virus first isolated by the Uganda Virus Research Institute in Entebbe, Uganda in 1959. It is a togavirus (family Togaviridae), genus Alphavirus and is closely related to Chikungunya and Igbo Ora viruses. The name comes from the Nilotic language of Uganda and Sudan and means “weakening of the joints.”
O'nyong'nyong virus is transmitted by bites from an infected mosquito. It is the only virus whose primary vectors are anopheline mosquitoes (Anopheles funestus and Anopheles gambiae).
Common symptoms of infection with the virus are polyarthritis, rash and fever. Other symptoms include eye pain, chest pain, lymphadenitis and lethargy. No fatalities due to infection are known.
There have been two epidemics of O’nyong’nyong fever. The first occurred from 1959-1962 spreading from Uganda to Kenya, Tanzania, Zaire (Democratic Republic of the Congo), Malawi and Mozambique, and affecting over two million people. This was one of the largest arbovirus epidemics recorded. The first virus isolates were obtained during this outbreak from mosquitoes and human blood samples collected from Gulu in northern Uganda in 1959.
The second epidemic in 1996-1997 affected 400 people and was confined to Uganda. The 35-year hiatus between the two outbreaks and evidence of an outbreak in 1904-1906 in Uganda indicates a 30-50 year cycle for epidemics.
The ONNV (o'nyong-nyong virus) has at least three major subtipes, or strains, which genomic sequences are currently available on genome databases.
O'nyong'nyong virus is transmitted by bites from an infected mosquito. It is the only virus whose primary vectors are anopheline mosquitoes (Anopheles funestus and Anopheles gambiae).
Common symptoms of infection with the virus are polyarthritis, rash and fever. Other symptoms include eye pain, chest pain, lymphadenitis and lethargy. No fatalities due to infection are known.
There have been two epidemics of O’nyong’nyong fever. The first occurred from 1959-1962 spreading from Uganda to Kenya, Tanzania, Zaire (Democratic Republic of the Congo), Malawi and Mozambique, and affecting over two million people. This was one of the largest arbovirus epidemics recorded. The first virus isolates were obtained during this outbreak from mosquitoes and human blood samples collected from Gulu in northern Uganda in 1959.
The second epidemic in 1996-1997 affected 400 people and was confined to Uganda. The 35-year hiatus between the two outbreaks and evidence of an outbreak in 1904-1906 in Uganda indicates a 30-50 year cycle for epidemics.
The ONNV (o'nyong-nyong virus) has at least three major subtipes, or strains, which genomic sequences are currently available on genome databases.
Flavivirus
Flavivirus is a genus of the family Flaviviridae. This genus includes the West Nile virus, dengue virus, Tick-borne Encephalitis Virus, Yellow Fever Virus, and several other viruses which may cause encephalitis.
Flavivirus share a common size (40-65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000-11,000 bases), and appearance in the electron microscope.
These viruses are transmitted by the bite from an infected arthropod (mosquito or tick) Human infections with these viruses are typically incidental, as humans are unable to replicate the virus to high enough titres to reinfect arthropods and thus continue the virus life cycle. The exceptions to this are Yellow fever virus and Dengue viruses which are well adapted to human and are not dependant upon any other hosts.
Other virus transmission routes include, handling infected animal carcases, blood transfusion, child birth and through consumption unpasturised milk products.
Animals are able to be infected with flavivirues, although the ability for these animals to directly transmit the virus is unlikely.
Flavivirus share a common size (40-65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000-11,000 bases), and appearance in the electron microscope.
These viruses are transmitted by the bite from an infected arthropod (mosquito or tick) Human infections with these viruses are typically incidental, as humans are unable to replicate the virus to high enough titres to reinfect arthropods and thus continue the virus life cycle. The exceptions to this are Yellow fever virus and Dengue viruses which are well adapted to human and are not dependant upon any other hosts.
Other virus transmission routes include, handling infected animal carcases, blood transfusion, child birth and through consumption unpasturised milk products.
Animals are able to be infected with flavivirues, although the ability for these animals to directly transmit the virus is unlikely.
(Courtesy of Xuan Le)bruce lee taking martial arts to protect himself from school bullies
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