Minggu, 30 November 2008
Sabtu, 22 November 2008
Chikungunya
Chikungunya adalah sejenis demam virus yang disebabkan alphavirus yang disebarkan oleh gigitan nyamuk dari spesies Aedes aegypti. Namanya berasal dari sebuah kata dalam bahasa Makonde yang berarti "yang melengkung ke atas", merujuk kepada tubuh yang membungkuk akibat gejala-gejala arthritis penyakit ini.
Penyakit ini pertama sekali dicatat di Tanzania, Afrika pada tahun 1952, kemudian di Uganda tahun 1963. Di Indonesia, kejadian luar biasa (KLB) Chikungunya dilaporkan pada tahun 1982 di beberapa provinsi: Yogyakarta (1983), Muara Enim (1999), Aceh dan Bogor (2001). Sebuah wabah Chikungunya ditemukan di Port Klang di Malaysia pada tahun 1999, menjangkiti 27 orang [1].
Gejala penyakit ini termasuk demam mendadak yang mencapai 39 derajat C, nyeri pada persendian terutama sendi lutut, pergelangan, jari kaki dan tangan serta tulang belakang yang disertai ruam (kumpulan bintik-bintik kemerahan) pada kulit. Terdapat juga sakit kepala, conjunctival injection dan sedikit fotofobia.
Ujian serologi untuk Chikungunya tersedia di Universitas Malaya di Kuala Lumpur, Malaysia.
Tidak terdapat sebarang rawatan khusus bagai Chikungunya. Penyakit ini biasanya dapat membatasi diri sendir dan akan sembuh sendiri. Perawatan berdasarkan gejala disarankan setelah mengetepikan penyakit-penyakit lain yang lebih berbahaya.
Chikungunya virus
CHIK is responsible for extensive Aedes aegypti-transmitted urban disease in cities in Africa and major epidemics in Asia. The crippling arthralgia and frequent arthritis that accompany the fever and other systemic symptoms are clinically distinct. Several other togaviruses of the alphavirus genus (Ross River, O’nyong-nyong, etc) have been associated with a similar syndrome. CHIK activity in Asia has been documented since its isolation in Bangkok in 1958. Other countries which have reported CHIK activity include Cambodia, Vietnam, Myanmar, Sri Lanka, India, Indonesia, and the Philippines.
CHIK virus is transmitted in the savannahs and forests of tropical Africa by Aedes mosquitoes of the subgenera Stegomyia and Diceromyia. Aedes aegypti is an important vector in urban epidemics in both Africa and Asia.
Clinical Features
CHIK is an acute infection of abrupt onset, heralded by fever and severe arthralgia, followed by other constitutional symptoms and rash, and lasting for a period of 1-7 days. The incubation period is usually 2-3 days, with a range of 1-12 days. Fever rises abruptly, often reaching 39 to 40 degrees centigrade and accompanied by intermittent shaking chills. This acute phase lasts 2-3 days. The temperature may remit for 1-2 days, resulting in a "saddle-back" fever curve.
The arthralgias are polyarticular, migratory, and predominantly affect the small joints of the hands, wrists, ankles and feet, with lesser involvement of larger joints. Pain on movement is worse in the morning, improved by mild exercise, and exacerbated by strenous exercise. Swelling may occur, but fluid accumulation is uncommon. Patients with milder articular manifestations are usually symptom-free within a few weeks, but more severe cases require months to resolve entirely. Generalized myalgia, as well as back and shoulder pain, is common.
Cutaneous manifestations are typical with many patients presenting with a flush over the face and trunk. This is usually followed by a rash generally described as maculopapular. The trunks and limbs are commonly involved, but face, palms and soles may also show lesions. Pruritis or irritation may accompany the eruption.
During the acute disease, most patients will have headache, but it is not usually severe. Photophobia and retroorbital pain also occur but not severe. Conjunctival injection is present in some cases. Some patients will complain of sore throat and have pharyngitis on examination.
CHIK infection has a somewhat different picture in younger patients. Arthralgia and arthritis occur but are less prominent and last a shorter time. Rash may be less frequent; but in infants and younger children, prominent flushing and early appearance of maculopapular or urticarial eruption may be a useful indicator.
In Asia, several virus isolations have been made from severely ill children diagnosed as having haemorrhagic fever, similar to DHF.
Treatment
Supportive 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.
Diagnosis
The definitive diagnosis can only be made by laboratory means, but CHIK should be suspected when epidemic disease occurs with the characteristic triad of fever, rash and rheumatic manifestations.
Virus isolation is readily accomplished by inoculation of mosquito cell culture, mosquito, mammalian cell culture or suckling mice. Viremia will be present in most patients during the first 48 hours of disease and may be detected as late as day 4 in some patients.
Virus-specific IgM antibodies are readily detected by capture ELISA in patients recovering from CHIK infection and they persist in excess of 6 months. Haemagglutination inhibition (HI) antibodies appear with the cessation of viremia. All patients will be positive by day 5 to 7 of illness. Neutralization antibodies parallel HI antibodies.
Chikungunya IgM serology test is available in University Malaya.
Penyakit ini pertama sekali dicatat di Tanzania, Afrika pada tahun 1952, kemudian di Uganda tahun 1963. Di Indonesia, kejadian luar biasa (KLB) Chikungunya dilaporkan pada tahun 1982 di beberapa provinsi: Yogyakarta (1983), Muara Enim (1999), Aceh dan Bogor (2001). Sebuah wabah Chikungunya ditemukan di Port Klang di Malaysia pada tahun 1999, menjangkiti 27 orang [1].
Gejala penyakit ini termasuk demam mendadak yang mencapai 39 derajat C, nyeri pada persendian terutama sendi lutut, pergelangan, jari kaki dan tangan serta tulang belakang yang disertai ruam (kumpulan bintik-bintik kemerahan) pada kulit. Terdapat juga sakit kepala, conjunctival injection dan sedikit fotofobia.
Ujian serologi untuk Chikungunya tersedia di Universitas Malaya di Kuala Lumpur, Malaysia.
Tidak terdapat sebarang rawatan khusus bagai Chikungunya. Penyakit ini biasanya dapat membatasi diri sendir dan akan sembuh sendiri. Perawatan berdasarkan gejala disarankan setelah mengetepikan penyakit-penyakit lain yang lebih berbahaya.
Chikungunya virus
CHIK is responsible for extensive Aedes aegypti-transmitted urban disease in cities in Africa and major epidemics in Asia. The crippling arthralgia and frequent arthritis that accompany the fever and other systemic symptoms are clinically distinct. Several other togaviruses of the alphavirus genus (Ross River, O’nyong-nyong, etc) have been associated with a similar syndrome. CHIK activity in Asia has been documented since its isolation in Bangkok in 1958. Other countries which have reported CHIK activity include Cambodia, Vietnam, Myanmar, Sri Lanka, India, Indonesia, and the Philippines.
CHIK virus is transmitted in the savannahs and forests of tropical Africa by Aedes mosquitoes of the subgenera Stegomyia and Diceromyia. Aedes aegypti is an important vector in urban epidemics in both Africa and Asia.
Clinical Features
CHIK is an acute infection of abrupt onset, heralded by fever and severe arthralgia, followed by other constitutional symptoms and rash, and lasting for a period of 1-7 days. The incubation period is usually 2-3 days, with a range of 1-12 days. Fever rises abruptly, often reaching 39 to 40 degrees centigrade and accompanied by intermittent shaking chills. This acute phase lasts 2-3 days. The temperature may remit for 1-2 days, resulting in a "saddle-back" fever curve.
The arthralgias are polyarticular, migratory, and predominantly affect the small joints of the hands, wrists, ankles and feet, with lesser involvement of larger joints. Pain on movement is worse in the morning, improved by mild exercise, and exacerbated by strenous exercise. Swelling may occur, but fluid accumulation is uncommon. Patients with milder articular manifestations are usually symptom-free within a few weeks, but more severe cases require months to resolve entirely. Generalized myalgia, as well as back and shoulder pain, is common.
Cutaneous manifestations are typical with many patients presenting with a flush over the face and trunk. This is usually followed by a rash generally described as maculopapular. The trunks and limbs are commonly involved, but face, palms and soles may also show lesions. Pruritis or irritation may accompany the eruption.
During the acute disease, most patients will have headache, but it is not usually severe. Photophobia and retroorbital pain also occur but not severe. Conjunctival injection is present in some cases. Some patients will complain of sore throat and have pharyngitis on examination.
CHIK infection has a somewhat different picture in younger patients. Arthralgia and arthritis occur but are less prominent and last a shorter time. Rash may be less frequent; but in infants and younger children, prominent flushing and early appearance of maculopapular or urticarial eruption may be a useful indicator.
In Asia, several virus isolations have been made from severely ill children diagnosed as having haemorrhagic fever, similar to DHF.
Treatment
Supportive 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.
Diagnosis
The definitive diagnosis can only be made by laboratory means, but CHIK should be suspected when epidemic disease occurs with the characteristic triad of fever, rash and rheumatic manifestations.
Virus isolation is readily accomplished by inoculation of mosquito cell culture, mosquito, mammalian cell culture or suckling mice. Viremia will be present in most patients during the first 48 hours of disease and may be detected as late as day 4 in some patients.
Virus-specific IgM antibodies are readily detected by capture ELISA in patients recovering from CHIK infection and they persist in excess of 6 months. Haemagglutination inhibition (HI) antibodies appear with the cessation of viremia. All patients will be positive by day 5 to 7 of illness. Neutralization antibodies parallel HI antibodies.
Chikungunya IgM serology test is available in University Malaya.
DENGUE FEVER (DEMAM BERDARAH)
Dengue fever
Dengue fever (pronounced /ˈdɛŋgeɪ/ (BrE), /ˈdɛŋgiː/ (AmE)) 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] It is also known as breakbone fever. The geographical spread is similar to malaria, but unlike malaria, dengue is often found in urban areas of tropical nations, including Puerto Rico, Singapore, Malaysia, Taiwan, Thailand, Indonesia, Philippines, Pakistan, India, Brazil, Vietnam, Guyana, Venezuela and Bangladesh. 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.
Signs and symptoms
This is manifested by a sudden onset of severe headache, muscle and joint pains (myalgias and arthralgias—severe pain gives it the name break-bone fever or bonecrusher disease), fever, and rash.[3] 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.
Some cases develop much milder symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present. Thus travelers from tropical areas may pass on dengue in their home countries inadvertently, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile.
The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called biphasic pattern). Clinically, the platelet count will drop until the patient's temperature is normal.
Cases of DHF also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.
[edit] Diagnosis
The 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.
The WHO definition of dengue haemorrhagic fever has been in use since 1975; all four criteria must be fulfilled:[4]
1. Fever, bladder problem, constant headaches, severe dizziness and loss of appetite.
2. Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)
3. Thrombocytopenia (<100,000 platelets per mm³ or estimated as less than 3 platelets per high power field)
4. 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, hypoproteinemia)
Dengue shock syndrome is defined as dengue hemorrhagic fever plus:
* Weak rapid pulse,
* Narrow pulse pressure (less than 20 mm Hg)
* Cold, clammy skin and restlessness.
Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated.
[edit] Treatment
The mainstay of treatment is timely supportive therapy to tackle shock due to haemoconcentration and bleeding. Close monitoring of vital signs in critical period (between day 2 to day 7 of fever) is vital. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant concentration of the blood if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion.
Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these drugs may worsen the bleeding tendency associated with some of these infections. Patients may receive paracetamol preparations to deal with these symptoms if dengue is suspected.[5]
[edit] Emerging treatments
Emerging evidence suggests that mycophenolic acid and ribavirin inhibit dengue replication. Initial experiments showed a fivefold increase in defective viral RNA production by cells treated with each drug.[6] In vivo studies, however, have not yet been done. Unlike HIV therapy, lack of adequate global interest and funding greatly hampers the development of treatment regime.
[edit] Epidemiology
World-wide dengue distribution, 2006. Red: Epidemic dengue. Blue: Aedes aegypti.
World-wide dengue distribution, 2000.
The first epidemics occurred almost simultaneously in Asia, Africa, and North America in the 1780s. The disease was identified and named (see #History below) in 1779. A global pandemic began in Southeast Asia in the 1950s and by 1975 DHF had become a leading cause of death among many children in many countries in that region. Epidemic dengue has become more common since the 1980s. By the late 1990s, dengue was the most important mosquito-borne disease affecting humans after malaria, there being around 40 million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each year. There was a serious outbreak in Rio de Janeiro in February 2002 affecting around one million people and killing sixteen.
On March 20, 2008, the secretary of health of the state of Rio de Janeiro, Sérgio Côrtes, announced that 23,555 cases of dengue, including 30 deaths, had been recorded in the state in less than three months. Côrtes said, "I am treating this as an epidemic because the number of cases is extremely high." Federal Minister of Health José Gomes Temporão also announced that he was forming a panel to respond to the situation. Cesar Maia, mayor of the city of Rio de Janeiro, denied that there was serious cause for concern, saying that the incidence of cases was in fact declining from a peak at the beginning of February. [7] By April 3, 2008, the number of cases reported rose to 55,000 [8]
Significant outbreaks of dengue fever tend to occur every five or six months. The cyclicity in numbers of dengue cases is thought to be the result of seasonal cycles interacting with a short-lived cross-immunity for all four strains, in people who have had dengue (Wearing and Rohani 2006). When the cross-immunity wears off, the population is then more susceptible to transmission whenever the next seasonal peak occurs. Thus in the longer term of several years, there tend to remain large numbers of susceptible people in the population despite previous outbreaks because there are four different strains of the dengue virus and because of new susceptible individuals entering the target population, either through childbirth or immigration.
There is significant evidence, originally suggested by S.B. Halstead in the 1970s, that dengue hemorrhagic fever is more likely to occur in patients who have secondary infections by serotypes different from the primary infection. One model to explain this process is known as antibody-dependent enhancement (ADE), which allows for increased uptake and virion replication during a secondary infection with a different strain. Through an immunological phenomenon, known as original antigenic sin, the immune system is not able to adequately respond to the stronger infection, and the secondary infection becomes far more serious.[9] This process is also known as superinfection.[10][11]
In Singapore, there are about 4,000–5,000 reported cases of dengue fever or dengue haemorrhagic fever every year. In the year 2003, there were six deaths from dengue shock syndrome.[citation needed] It is believed that the reported cases of dengue are an underrepresentation of all the cases of dengue as it would ignore subclinical cases and cases where the patient did not present for medical treatment. With proper medical treatment, the mortality rate for dengue can therefore be brought down to less than 1 in 1000
Dengue fever (pronounced /ˈdɛŋgeɪ/ (BrE), /ˈdɛŋgiː/ (AmE)) 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] It is also known as breakbone fever. The geographical spread is similar to malaria, but unlike malaria, dengue is often found in urban areas of tropical nations, including Puerto Rico, Singapore, Malaysia, Taiwan, Thailand, Indonesia, Philippines, Pakistan, India, Brazil, Vietnam, Guyana, Venezuela and Bangladesh. 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.
Signs and symptoms
This is manifested by a sudden onset of severe headache, muscle and joint pains (myalgias and arthralgias—severe pain gives it the name break-bone fever or bonecrusher disease), fever, and rash.[3] 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.
Some cases develop much milder symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present. Thus travelers from tropical areas may pass on dengue in their home countries inadvertently, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile.
The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called biphasic pattern). Clinically, the platelet count will drop until the patient's temperature is normal.
Cases of DHF also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.
[edit] Diagnosis
The 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.
The WHO definition of dengue haemorrhagic fever has been in use since 1975; all four criteria must be fulfilled:[4]
1. Fever, bladder problem, constant headaches, severe dizziness and loss of appetite.
2. Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)
3. Thrombocytopenia (<100,000 platelets per mm³ or estimated as less than 3 platelets per high power field)
4. 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, hypoproteinemia)
Dengue shock syndrome is defined as dengue hemorrhagic fever plus:
* Weak rapid pulse,
* Narrow pulse pressure (less than 20 mm Hg)
* Cold, clammy skin and restlessness.
Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated.
[edit] Treatment
The mainstay of treatment is timely supportive therapy to tackle shock due to haemoconcentration and bleeding. Close monitoring of vital signs in critical period (between day 2 to day 7 of fever) is vital. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant concentration of the blood if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion.
Aspirin and non-steroidal anti-inflammatory drugs should be avoided as these drugs may worsen the bleeding tendency associated with some of these infections. Patients may receive paracetamol preparations to deal with these symptoms if dengue is suspected.[5]
[edit] Emerging treatments
Emerging evidence suggests that mycophenolic acid and ribavirin inhibit dengue replication. Initial experiments showed a fivefold increase in defective viral RNA production by cells treated with each drug.[6] In vivo studies, however, have not yet been done. Unlike HIV therapy, lack of adequate global interest and funding greatly hampers the development of treatment regime.
[edit] Epidemiology
World-wide dengue distribution, 2006. Red: Epidemic dengue. Blue: Aedes aegypti.
World-wide dengue distribution, 2000.
The first epidemics occurred almost simultaneously in Asia, Africa, and North America in the 1780s. The disease was identified and named (see #History below) in 1779. A global pandemic began in Southeast Asia in the 1950s and by 1975 DHF had become a leading cause of death among many children in many countries in that region. Epidemic dengue has become more common since the 1980s. By the late 1990s, dengue was the most important mosquito-borne disease affecting humans after malaria, there being around 40 million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each year. There was a serious outbreak in Rio de Janeiro in February 2002 affecting around one million people and killing sixteen.
On March 20, 2008, the secretary of health of the state of Rio de Janeiro, Sérgio Côrtes, announced that 23,555 cases of dengue, including 30 deaths, had been recorded in the state in less than three months. Côrtes said, "I am treating this as an epidemic because the number of cases is extremely high." Federal Minister of Health José Gomes Temporão also announced that he was forming a panel to respond to the situation. Cesar Maia, mayor of the city of Rio de Janeiro, denied that there was serious cause for concern, saying that the incidence of cases was in fact declining from a peak at the beginning of February. [7] By April 3, 2008, the number of cases reported rose to 55,000 [8]
Significant outbreaks of dengue fever tend to occur every five or six months. The cyclicity in numbers of dengue cases is thought to be the result of seasonal cycles interacting with a short-lived cross-immunity for all four strains, in people who have had dengue (Wearing and Rohani 2006). When the cross-immunity wears off, the population is then more susceptible to transmission whenever the next seasonal peak occurs. Thus in the longer term of several years, there tend to remain large numbers of susceptible people in the population despite previous outbreaks because there are four different strains of the dengue virus and because of new susceptible individuals entering the target population, either through childbirth or immigration.
There is significant evidence, originally suggested by S.B. Halstead in the 1970s, that dengue hemorrhagic fever is more likely to occur in patients who have secondary infections by serotypes different from the primary infection. One model to explain this process is known as antibody-dependent enhancement (ADE), which allows for increased uptake and virion replication during a secondary infection with a different strain. Through an immunological phenomenon, known as original antigenic sin, the immune system is not able to adequately respond to the stronger infection, and the secondary infection becomes far more serious.[9] This process is also known as superinfection.[10][11]
In Singapore, there are about 4,000–5,000 reported cases of dengue fever or dengue haemorrhagic fever every year. In the year 2003, there were six deaths from dengue shock syndrome.[citation needed] It is believed that the reported cases of dengue are an underrepresentation of all the cases of dengue as it would ignore subclinical cases and cases where the patient did not present for medical treatment. With proper medical treatment, the mortality rate for dengue can therefore be brought down to less than 1 in 1000
BIRD FLU
Avian influenza, sometimes Avian flu, and commonly Bird flu refers to "influenza caused by viruses adapted to birds.
"Bird flu" is a phrase similar to "Swine flu", "Dog flu", "Horse flu", or "Human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species: Influenza A virus. All subtypes (but not all strains of all subtypes) of Influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the Influenza A virus (note that the "A" does not stand for "avian").
Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish Flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly later pandemic strains.
Genetics
Genetic factors in distinguishing between "human flu viruses" and "avian flu viruses" include:
PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine.
HA: (hemagglutinin): Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors. Hemagglutinin is the major antigen of the virus against which neutralizing antibodies are produced and influenza virus epidemics are associated with changes in its antigenic structure.
Influenza pandemic
Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both the H2N2 and H3N2 pandemic strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible.[8] The Spanish flu virus strain may have been transmitted directly from birds to humans.[9]
In spite of their pandemic connection, avian influenza viruses are noninfectious for most species. When they are infectious they are usually asymptomatic, so the carrier does not have any disease from it. Thus while infected with an avian flu virus, the animal doesn't have a "flu". Typically, when illness (called "flu") from an avian flu virus does occur, it is the result of an avian flu virus strain adapted to one species spreading to another species (usually from one bird species to another bird species). So far as is known, the most common result of this is an illness so minor as to be not worth noticing (and thus little studied). But with the domestication of chickens and turkeys, humans have created species subtypes (domesticated poultry) that can catch an avian flu virus adapted to waterfowl and have it rapidly mutate into a form that kills in days over 90% of an entire flock and spread to other flocks and kill 90% of them and can only be stopped by killing every domestic bird in the area. Until H5N1 infected humans in the 1990s, this was the only reason avian flu was considered important. Since then, avian flu viruses have been intensively studied; resulting in changes in what is believed about flu pandemics, changes in poultry farming, changes in flu vaccination research, and changes in flu pandemic planning.
H5N1 has evolved into a flu virus strain that infects more species than any previously known flu virus strain, is deadlier than any previously known flu virus strain, and continues to evolve becoming both more widespread and more deadly causing Robert Webster, a leading expert on avian flu, to publish an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist. He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives.[10] Since the article was written, the world community has spent billions of dollars fighting this threat with limited success.
"Bird flu" is a phrase similar to "Swine flu", "Dog flu", "Horse flu", or "Human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species: Influenza A virus. All subtypes (but not all strains of all subtypes) of Influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the Influenza A virus (note that the "A" does not stand for "avian").
Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish Flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly later pandemic strains.
Genetics
Genetic factors in distinguishing between "human flu viruses" and "avian flu viruses" include:
PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine.
HA: (hemagglutinin): Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors. Hemagglutinin is the major antigen of the virus against which neutralizing antibodies are produced and influenza virus epidemics are associated with changes in its antigenic structure.
Influenza pandemic
Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both the H2N2 and H3N2 pandemic strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible.[8] The Spanish flu virus strain may have been transmitted directly from birds to humans.[9]
In spite of their pandemic connection, avian influenza viruses are noninfectious for most species. When they are infectious they are usually asymptomatic, so the carrier does not have any disease from it. Thus while infected with an avian flu virus, the animal doesn't have a "flu". Typically, when illness (called "flu") from an avian flu virus does occur, it is the result of an avian flu virus strain adapted to one species spreading to another species (usually from one bird species to another bird species). So far as is known, the most common result of this is an illness so minor as to be not worth noticing (and thus little studied). But with the domestication of chickens and turkeys, humans have created species subtypes (domesticated poultry) that can catch an avian flu virus adapted to waterfowl and have it rapidly mutate into a form that kills in days over 90% of an entire flock and spread to other flocks and kill 90% of them and can only be stopped by killing every domestic bird in the area. Until H5N1 infected humans in the 1990s, this was the only reason avian flu was considered important. Since then, avian flu viruses have been intensively studied; resulting in changes in what is believed about flu pandemics, changes in poultry farming, changes in flu vaccination research, and changes in flu pandemic planning.
H5N1 has evolved into a flu virus strain that infects more species than any previously known flu virus strain, is deadlier than any previously known flu virus strain, and continues to evolve becoming both more widespread and more deadly causing Robert Webster, a leading expert on avian flu, to publish an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist. He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives.[10] Since the article was written, the world community has spent billions of dollars fighting this threat with limited success.
MAD COW
Bovine spongiform encephalopathy
Bovine Spongiform Encephalopathy (BSE), commonly known as Mad-Cow Disease (MCD), is a fatal, neurodegenerative disease in cattle, that causes a spongy degeneration in the brain and spinal cord and also causes red eyes. BSE has a long incubation period, about 4 years, usually affecting adult cattle at a peak age onset of four to five years, all breeds being equally susceptible.[1] In the United Kingdom, the country worst affected, more than 179,000 cattle have been infected and 4.4 million slaughtered during the eradication programme.[2]
It is believed by most scientists that the disease may be transmitted to human beings who eat the brain or spinal cord of infected carcasses.[3] In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by April 2008, it had killed 164 people in Britain, and 40 elsewhere[4] with the number expected to rise because of the disease's long incubation period.[5] Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989.[6]
A British inquiry into BSE concluded that the epidemic was caused by cattle, who are normally herbivores, being fed the remains of other cattle in the form of meat and bone meal (MBM), which caused the infectious agent to spread.[7][8] The origin of the disease itself remains unknown. The infectious agent is distinctive for the high temperatures at which it remains viable; this contributed to the spread of the disease in Britain, which had reduced the temperatures used during its rendering process.[7] Another contributory factor was the feeding of infected protein supplements to very young
Bovine Spongiform Encephalopathy (BSE), commonly known as Mad-Cow Disease (MCD), is a fatal, neurodegenerative disease in cattle, that causes a spongy degeneration in the brain and spinal cord and also causes red eyes. BSE has a long incubation period, about 4 years, usually affecting adult cattle at a peak age onset of four to five years, all breeds being equally susceptible.[1] In the United Kingdom, the country worst affected, more than 179,000 cattle have been infected and 4.4 million slaughtered during the eradication programme.[2]
It is believed by most scientists that the disease may be transmitted to human beings who eat the brain or spinal cord of infected carcasses.[3] In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by April 2008, it had killed 164 people in Britain, and 40 elsewhere[4] with the number expected to rise because of the disease's long incubation period.[5] Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989.[6]
A British inquiry into BSE concluded that the epidemic was caused by cattle, who are normally herbivores, being fed the remains of other cattle in the form of meat and bone meal (MBM), which caused the infectious agent to spread.[7][8] The origin of the disease itself remains unknown. The infectious agent is distinctive for the high temperatures at which it remains viable; this contributed to the spread of the disease in Britain, which had reduced the temperatures used during its rendering process.[7] Another contributory factor was the feeding of infected protein supplements to very young
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