The scientists at the University of Queensland, Brisbane, have shown that mosquitoes infected with Wolbachia live an average of only 27 days in contrast to the average longevity of 61 days for those not infected with the bacteria…..CLICK & SEE
Female mosquitoes infected with the bacteria transmit it to their offspring. “This may allow a small seed population of infected mosquitoes to grow into large numbers over time,” Scott ’Neill, the research team leader, told The Telegraph.
The shortened lives of the infected mosquitoes reduce their opportunity to spread disease-causing viruses. Most viruses transmitted by mosquitoes require about two weeks to incubate inside the insects before they are ready to be spread through bites. Mosquitoes whose life spans have been slashed by half won’t have enough time to spread the infection.
The vertical transmission of Wolbachia from female mosquitoes to offspring will be the key to successful spread of the infected mosquitoes, ’Neill said.
Experiments by ’Neill and his colleagues showed that 99 per cent of larvae from a group of infected females carried the infection.
But the experiments were done in closed environments and scientists are yet to develop an effective mechanism to introduce such infected mosquitoes in the wild.
“Modelling studies suggest that if we can infect about 0.4 per cent of mosquitoes, the infected population will establish itself,” ’Neill said.
Definition:
Yellow fever (also called yellow jack, black vomit or sometimes American Plague) is an acute viral disease. It is an important cause of hemorrhagic illness in many African and South American countries despite existence of an effective vaccine. The yellow refers to the jaundice symptoms that affect some patients.It is a viral infection transmitted by mosquitoes.
Yellow fever is a viral hemorrhagic fever caused by the yellow fever virus. The yellow fever virus is a single-stranded enveloped virus that belongs to the flavivirus group. The disease can result in mild symptoms or severe illness and death (mortality rate 5-70%). Yellow fever derives its name from the yellowing of the skin and whites of the eyes (jaundice) that occur in some people infected with the virus. Jaundice is caused by the presence of bile pigment (bilirubin) in the bloodstream and results from damage to liver cells (hepatocytes) during severe infection.…click & see
The yellow fever virus infects mainly monkeys and humans: monkeys are the animal reservoir. Infection is transmitted from human to human, monkey to monkey, monkey to human, and human to monkey by daytime-biting mosquitos. Several species of Aedes and Haemoagogus mosquitos can serve as vectors, transmitting the virus during a blood meal.
Three types of transmission cycles exist for yellow fever: sylvatic (jungle), intermediate and urban. Although all three transmission cycles occur in Africa, only sylvatic and urban transmission cycles occur in South America.
* Occurs in monkeys infected by wild mosquitos in tropical rainforests
* Infected monkeys pass the virus to mosquitos during feeding
* Infected wild mosquitos bite humans entering the rainforest (accidental infection)
Intermediate yellow fever (monkey to human; human to monkey)
* Small-scale epidemics that occur in humid or semi-humid grasslands of Africa
* Separate villages experience simultaneous infections transmitted by semi-domestic mosquitos that infect both monkey and human hosts
* Most common type of outbreak in Africa
Urban yellow fever (human to human)
* Large epidemics occurring when the virus is introduced into high human population areas by migrants
* Domestic mosquitos of one species (Aedes aegypti) transmit the virus from person to person
* Monkeys are not involved in transmission
* Outbreaks spread from one source to cover a wide area
Yellow fever has been a source of several devastating epidemics. Yellow fever epidemics broke out in the 1700s in Italy, France, Spain, and England. 300,000 people are believed to have died from yellow fever in Spain during the 19th century. French soldiers were attacked by yellow fever during the 1802 Haitian Revolution; more than half of the army perished from the disease. Outbreaks followed by thousands of deaths occurred periodically in other Western Hemisphere locations until research, which included human volunteers (some of whom died), led to an understanding of the method of transmission to humans (primarily by mosquitos) and development of a vaccine and other preventive efforts in the early 20th century.
Despite the costly and sacrificial breakthrough research by Cuban physician Carlos Finlay, American physician Walter Reed, and many others over 100 years ago, unvaccinated populations in many developing nations in Africa and Central and South America continue to be at risk. As of 2001, the World Health Organization (WHO) estimates that yellow fever causes 200,000 illnesses and 30,000 deaths every year in unvaccinated populations.
Causes :-
Yellow fever is caused by a small virus that is spread by the bite of mosquitoes. This disease is common in South America and in sub-Saharan Africa.
Anyone can get yellow fever, but the elderly have a higher risk of severe infection. If a person is bitten by an infected mosquito, symptoms usually develop 3 – 6 days later.
Yellow fever has three stages:
1.Early stage: Headache, muscle aches, fever, loss of appetite, vomiting, and jaundice are common. After approximately 3 – 4 days, often symptoms go away briefly (remission).
2.Period of remission: After 3 – 4 days, fever and other symptoms go away. Most people will recover at this stage, but others may move onto the third, most dangerous stage (intoxication stage) within 24 hours.
3.Period of intoxication: Multi-organ dysfunction occurs. This includes liver and kidney failure, bleeding disorders/hemorrhage, and brain dysfunction including delirium, seizures, coma, shock, and death.
Although viral replication begins in cells at the site of the mosquito bite, symptoms of infection are not usually noted for a period of three to six days when the acute phase of infection presents. Acute yellow fever infection is characterized by high fever, muscle pain, backache, headache, shivers, loss of appetite, nausea and/or vomiting. Most people infected improve after three to four days.
However, within 24 hours of the disappearance of symptoms, up to 15% of those infected enter a toxic phase during which fever resumes, and the yellow fever virus quickly spreads to the kidneys, lymph nodes, spleen, bone marrow and liver. Liver invasion of one of the last stages to occur: as the liver is increasingly damaged, patients develop jaundice as bilirubin is released from damaged liver cells, experience abdominal pain and vomiting, and develop coagulopathies (inability of the blood to clot) characterized by bleeding from the mouth, nose, eyes and stomach, and presence of blood in vomit and stool. Up to 50% of people who enter the toxic phase die within two weeks of infection.
Diagnosis:-
Yellow fever may be difficult to diagnose, especially during the early stages, and may be confused with malaria, typhoid, other hemorrhagic fevers (dengue, Rift Valley, Venezuelan, Bolivian, Argentine, Lassa, Crimean-Congo, Marburg and Ebola), rickettsial infection, leptospirosis, viral hepatitis, other causes of liver failure and toxic hepatitis (e.g. carbon-tetrachloride poisoning).
Exams and Tests
A person with advanced yellow fever may show signs of liver failure, renal failure, and shock.
If you have symptoms of yellow fever, tell your doctor if you have traveled to areas where the disease is known to thrive. Blood tests can confirm the diagnosis.
Treatment :-
There is no specific treatment for yellow fever. Treatment for symptoms can include:
*Blood products for severe bleeding
*Dialysis for kidney failure
*Fluids through a vein (intravenous fluids)
The treatment for yellow fever is supportive: control of fever, fluids to treat dehydration, and intensive support related to organ damage.
The World Health Organization estimates 200,000 cases of yellow fever per year with approximately 30,000 deaths.
Yellow fever ranges in severity. Severe infections with internal bleeding and fever (hemorrhagic fever) are deadly in up to half of cases.
Historical reports have claimed a mortality rate of between 1 in 17 (5.8%) and 1 in 3 (33%). CDC has claimed that case-fatality rates from severe disease range from 15% to more than 50%. The WHO factsheet on yellow fever, updated in 2001, states that 15% of patients enter a “toxic phase” and that half of that number die within ten to fourteen days, with the other half recovering
If you will be traveling to an area where yellow fever is common:
*Sleep in screened housing
*Use mosquito repellents
*Wear clothing that fully covers your body
*There is an effective vaccine against yellow fever. Ask your doctor at least 10 – 14 days before traveling if you should be *vaccinated against yellow fever.
In 1937, Max Theiler, working at the Rockefeller Foundation, developed a safe and highly efficacious vaccine for yellow fever that gives a ten-year or more immunity from the virus. The vaccine consists of a live, but attenuated, virus called 17D. The 17D vaccine has been used commercially since the 1950s. The mechanisms of attenuation and immunogenicity for the 17D strain are not known. However, this vaccine is very safe, with few adverse reactions having been reported and millions of doses administered, and highly effective with over 90% of vaccinees developing a measurable immune response after the first dose.
Although the vaccine is considered safe, there are risks involved. The majority of adverse reactions to the 17D vaccine result from allergic reaction to the eggs in which the vaccine is grown. Persons with a known egg allergy should discuss this with their physician prior to vaccination. In addition, there is a small risk of neurologic disease and encephalitis, particularly in individuals with compromised immune systems and very young children. The 17D vaccine is contraindicated in infants, pregnant women, and anyone with a diminished immune capacity, including those taking immunosuppressant drugs.
According to the travel clinic at the University of Utah Hospital, the vaccine presents an increased risk of adverse reaction in adults aged 60 and older, with the risk increasing again after age 65, and again after age 70. The reaction is capable of producing multiple organ failure and should be evaluated carefully by a qualified health professional before being administered to the elderly.
Finally, there is a very small risk of more severe yellow fever-like disease associated with the vaccine. This reaction occurs in 1~3 vaccinees per million doses administered. This reaction, called YEL-AVD, causes a fairly severe disease closely resembling yellow fever caused by virulent strains of the virus. The risk factor/s for YEL-AVD are not known, although it has been suggested that it may be genetic. The 2`-5` oligoadenylate synthetase (OAS) component of the innate immune response has been shown to be particularly important in protection from Flavivirus infection. In at least one case of YEL-AVD, the patient was found to have an allelic mutation in a single nucleotide polymorphism (SNP) of the OAS gene. People most at risk of contracting the virus should be vaccinated. Woodcutters working in tropical areas should be particularly targeted for vaccination. Insecticides, protective clothing, and screening of houses are helpful, but not always sufficient for mosquito control; people should always use an insecticide spray while in certain areas. In affected areas, mosquito control methods have proven effective in decreasing the number of cases.
Recent studies have noted the increase in the number of areas affected by a number of mosquito-borne viral infections and have called for further research and funding for vaccines
Current research:-
In the hamster model of yellow fever, early administration of the antiviral ribavirin is an effective early treatment of many pathological features of the disease. Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in target organs (liver and spleen), prevented hepatocellular steatosis, and normalized alanine aminotransferase (a liver damage marker) levels. The results of this study suggest that ribavirin may be effective in the early treatment of yellow fever, and that its mechanism of action in reducing liver pathology in yellow fever virus infection may be similar to that observed with ribavirin in the treatment of hepatitis C, a virus related to yellow fever. Because ribavirin had failed to improve survival in a virulent primate (rhesus) model of yellow fever infection, it had been previously discounted as a possible therapy.
In 2007, the World Community Grid launched a project whereby computer modelling of the yellow fever virus (and related viruses), thousands of small molecules are screened for their potential anti-viral properties in fighting yellow fever. This is the first project to utilize computer simulations in seeking out medicines to directly attack the virus once a person is infected. This is a distributed process project similar to SETI@Home where the general public downloads the World Community Grid agent and the program (along with thousands of other users) screens thousands of molecules while their computer would be otherwise idle. If the user needs to use the computer the program sleeps. There are several different projects running, including a similar one screening for anti-AIDS drugs. The project covering yellow fever is called “Discovering Dengue Drugs – Together.” The software and information about the project can be found at: World Community Grid web site
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose. Resources:
http://en.wikipedia.org/wiki/Yellow_fever
http://www.nlm.nih.gov/medlineplus/ency/article/001365.htm
http://microbiology.suite101.com/article.cfm/yellow_fever
Other Names:Weil’s disease, canicola fever, canefield fever, nanukayami fever, 7-day fever and many more
Definition:Leptospirosis is an infectious disease caused by a particular type of bacteria called a spirochete. Leptospirosis can be transmitted by many animals such as rats, skunks, opossums, raccoons, foxes, and other vermin.The infection is commonly transmitted to humans by allowing fresh water that has been contaminated by animal urine to come in contact with unhealed breaks in the skin, eyes or with the mucous membranes. Outside of tropical areas, leptospirosis cases have a relatively distinct seasonality with most of them occurring August-September/February-March. The soil or water is contaminated with the waste products of an infected animal. People contract the disease by either ingesting contaminated food or water or by broken skin and mucous membrane (eyes, nose, sinuses, mouth) contact with the contaminated water or soil.
Though being recognised among the world’s most common zoonoses, leptospirosis is a relatively rare bacterial infection in humans.
Leptospirosis occurs worldwide, but it is most commonly acquired in the tropics. The U.S. Centers for Disease Control and Prevention states 100-200 cases of leptospirosis are reported each year in the United States, with about 50% of cases occurring in Hawaii.
Causes:
Leptospirosis is caused by a spirochaete bacterium called Leptospira spp. that has at 5 different serovars of importance in the United States causing disease (icterohaemorrhagiae, canicola, pomona, grippotyphosa, and bratislava). There are other (less common) infectious strains. It should however be noted that genetically different leptospira organisms may be identical serologically and vice versa. Hence, an argument exists on the basis of strain identification. The traditional serologic system is seemingly more useful from diagnostic and epidemiologic standpoint at the moment (which may change with further development and spread of technologies like PCR).
Leptospirosis is transmitted by the urine of an infected animal, and is contagious as long as it is still moist. Although rats, mice and voles are important primary hosts, a wide range of other mammals including dogs, deer, rabbits, hedgehogs, cows, sheep, raccoons, possums, skunks, and even certain marine mammals are also able to carry and transmit the disease as secondary hosts. Dogs may lick the urine of an infected animal off the grass or soil, or drink from an infected puddle. There have been reports of “house dogs” contracting leptospirosis apparently from licking the urine of infected mice that entered the house. The type of habitats most likely to carry infective bacteria are muddy riverbanks, ditches, gulleys and muddy livestock rearing areas where there is regular passage of either wild or farm mammals. There is a direct correlation between the amount of rainfall and the incidence of leptospirosis, making it seasonal in temperate climates and year-round in tropical climates.
Leptospirosis is also transmitted by the semen of infected animals. Abattoir workers can contract the disease through contact with infected blood or body fluids.
Humans become infected through contact with water, food, or soil containing urine from these infected animals. This may happen by swallowing contaminated food or water or through skin contact. The disease is not known to be spread from person to person and cases of bacterial dissemination in convalescence are extremely rare in humans. Leptospirosis is common among watersport enthusiasts in specific areas as prolonged immersion in water is known to promote the entry of the bacteria. Occupational risk factors include veterinarians, slaughter house workers, farmers, sewer workers, and architects and other building workers working on derelict buildings. An outbreak in an inner city environment has been linked to contact with rat urine.
Symptoms:
In humans, leptospiral infection causes a wide range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins with flu-like symptoms (fever, chills, myalgias, intense headache). The first phase resolves and the patient is asymptomatic briefly before the second phase begins that is characterized by meningitis, liver damage (causing jaundice), and renal failure. Because of the wide range of symptoms the infection is often wrongly diagnosed. This leads to a lower registered number of cases than there really are. Symptoms of leptospirosis include high fever, severe headache, chills, muscle aches, and vomiting, and may include jaundice, red eyes, abdominal pain, diarrhea, and/or a rash. The symptoms in humans appear after a 4-14 day incubation period.
Leptospirosis symptoms begin from two to 25 days after initial direct exposure to the urine or tissue of an infected animal. This can even occur via contaminated soil or water. Veterinarians, pet shop owners, sewage workers, and farm employees are at particularly high risk. People participating in outdoor sporting activities like canoeing, rafting, hiking, and camping can also come into contact with contaminated water or soil.
The illness typically progresses through two phases:
The first phase of nonspecific flulike symptoms includes headaches, muscle aches, eye pain with bright lights, followed by chills and fever. Watering and redness of the eyes occurs and symptoms seem to improve by the fifth to ninth day.
The second phase begins after a few days of feeling well. The initial symptoms recur with fever and aching with stiffness of the neck. Some patients develop serious inflammation of the nerves to the eyes, brain, spinal column (meningitis), or other nerves. Right upper area abdominal pain may occur. Less common symptoms relate to disease of the liver, lungs, kidneys, and heart.
Leptospirosis associated with liver and kidney disease is called Weil’s syndrome and is characterized by yellowing of the eyes (jaundice). Patients with Weil’s syndrome can also develop kidney disease and have more serious involvement of the organs affected.
Diagnosis:
The diagnosis of leptospirosis is made by culture of the bacterial organism Leptospira from infected blood, spinal fluid, or urine. However, many doctors must rely upon rising Leptospira antibody levels in the blood in order to make the diagnosis, as the technique required to perform the culturing is delicate and difficult.
Differential diagnosis list for leptospirosis is very large due to diverse symptomatics. For forms with middle to high severity, the list includes dengue fever and other hemorrhagic fevers, hepatitis of various etiologies, viral meningitis, malaria and typhoid fever. Light forms should be distinguished from influenza and other related viral diseases. Specific tests are a must for proper diagnosis of leptospirosis. Under circumstances of limited access (e.g., developing countries) to specific diagnostic means, close attention must be paid to anamnesis of the patient. Factors like certain dwelling areas, seasonality, contact with stagnant water (swimming, working on flooded meadows, etc) and/or rodents in the medical history support the leptospirosis hypothesis and serve as indications for specific tests (if available).
Leptospira can be cultured in Ellinghausen-McCullough-Johnson-Harris medium, which is incubated at 28 to 30°C. The median time to positivity is three weeks with a maximum of 3 months. This makes culture techniques useless for diagnostic purposes, but is commonly used in research.
Can my pets get leptospirosis?
According to the CDC, your pets (especially dogs, less commonly cats) can contract leptospirosis. Your pet can contract it in the same ways you can (ingesting contaminated soil, water or through skin wounds). Your pet may exhibit vomiting, refusal to eat, weight loss, decreased activity, muscle pains, or stiffness.
If you suspect your pet is ill, take them to a veterinarian for testing and treatment. Early antibiotic treatment often can limit or prevent organ damage.
If your pet is diagnosed with leptospirosis, you must be careful to try to prevent exposure to yourself or other household members. Remember to wash your hands frequently with soap and water after cleaning up waste from your pet. If possible, use latex or rubber gloves to do the job of clean up. Use a diluted (1:10 parts) bleach solution to clean surfaces where pet wastes may have contaminated. And make sure your pet receives the full course of antibiotic treatment that is prescribed by your vet. Discuss other pet-care issues directly with your vet should you have any other questions regarding the disease.
Treatment:
Leptospirosis treatment is a relatively complicated process comprising two main components – suppressing the causative agent and fighting possible complications. Aetiotropic drugs are antibiotics, such as cefotaxime, doxycycline, penicillin, ampicillin, and amoxicillin (doxycycline can also be used as a prophylaxis). There are no human vaccines; animal vaccines are only for a few strains, and are only effective for a few months. Human therapeutic dosage of drugs is as follows: doxycycline 100 mg orally every 12 hours for 1 week or penicillin 1-1.5 MU every 4 hours for 1 week. Doxycycline 200-250 mg once a week is administered as a prophylaxis. In dogs, penicillin is most commonly used to end the leptospiremic phase (infection of the blood), and doxycycline is used to eliminate the carrier state.
Supportive therapy measures (esp. in severe cases) include detoxication and normalization of the hydro-electrolytic balance. Glucose and salt solution infusions may be administered; dialysis is used in serious cases. Elevations of serum potassium are common and if the potassium level gets too high special measures must be taken. Serum phosphorus levels may likewise increase to unacceptable levels due to renal failure. Treatment for hyperphosphatemia consists of treating the underlying disease, dialysis where appropriate, or oral administration of calcium carbonate, but not without first checking the serum calcium levels (these two levels are related). Corticosteroids administration in gradually reduced doses (e.g., prednisolone starting from 30-60 mg) during 7-10 days is recommended by some specialists in cases of severe haemorrhagic effects.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Research
Leptospirosis: a zoonotic disease of global importance. Lancet Infect Dis. 2003 Dec;3(12):757-71 Bharti AR, Nally JE, Ricaldi JN, Matthias MA, Diaz MM, Lovett MA, Levett PN, Gilman RH, Willig MR, Gotuzzo E, Vinetz JM; Peru-United States Leptospirosis Consortium.
In the past decade, leptospirosis has emerged as a globally important infectious disease. It occurs in urban environments of industrialised and developing countries, as well as in rural regions worldwide. Mortality remains significant, related both to delays in diagnosis due to lack of infrastructure and adequate clinical suspicion, and to other poorly understood reasons that may include inherent pathogenicity of some leptospiral strains or genetically determined host immunopathological responses. Pulmonary haemorrhage is recognised increasingly as a major, often lethal, manifestation of leptospirosis, the pathogenesis of which remains unclear. The completion of the genome sequence of Leptospira interrogans serovar lai, and other continuing leptospiral genome sequencing projects, promise to guide future work on the disease. Mainstays of treatment are still tetracyclines and beta-lactam/cephalosporins. No vaccine is available. Prevention is largely dependent on sanitation measures that may be difficult to implement, especially in developing countries.
In a study of 38 dogs diagnosed and properly treated for leptospirosis published in the February 2000 issue of the Journal of the American Veterinary Association, the survival rate for the dialysis patients was slightly higher than the ones not put on dialysis, but both were in the 85% range (plus or minus). Of the dogs in this study that did not die, most recovered adequate kidney function, although one had chronic renal problems.
Dengue fever is a disease caused by a family of viruses that are transmitted by mosquitoes. It is an acute illness of sudden onset that usually follows a benign course with headache, fever, exhaustion, severe joint and muscle pain, swollen glands (lymphadenopathy), and rash. The presence (the “dengue triad”) of fever, rash, and headache (and other pains) is particularly characteristic of dengue.
Dengue (pronounced DENG-gay) strikes people with low levels of immunity. Because it is caused by one of four serotypes of virus, it is possible to get dengue fever multiple times. However, an attack of dengue produces immunity for a lifetime to that particular serotype to which the patient was exposed.
Dengue fever 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. 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, 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.
How is dengue contracted?
The virus is contracted from the bite of a striped Aedes aegypti mosquito that has previously bitten an infected person. The mosquito flourishes during rainy seasons but can breed in water-filled flower pots, plastic bags, and cans year-round.
One mosquito bite can inflict the disease.
The virus is not contagious and cannot be spread directly from person to person. There must be a person-to-mosquito-to-another-person pathway.
Signs & symptoms:
Dengue starts with chills, headache, pain upon moving the eyes, and low backache. Painful aching in the legs and joints occurs during the first hours of illness. The temperature rises quickly as high as 104° F (40° C), with relative low heart rate (bradycardia) and low blood pressure (hypotension). The eyes become reddened. A flushing or pale pink rash comes over the face and then disappears. The glands (lymph nodes) in the neck and groin are often swollen.
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This 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.
* uncontrollable laughing,
* extreme constipation
Some cases develop much milder symptoms which can, when no rash is present, be misdiagnosed as influenza or other viral infection. Thus travelers from tropical areas may inadvertently pass on dengue in their home countries, 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, haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.
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:
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) or,
* Cold, clammy skin and restlessness.
Serology and polymerase chain reaction (PCR) studies are available to confirm the diagnosis of dengue if clinically indicated.
Treatment:
Because dengue is caused by a virus, there is no specific medicine or antibiotic to treat it. For typical dengue, the treatment is purely concerned with relief of the symptoms (symptomatic).
The mainstay of treatment is supportive therapy. 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.
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. In vivo studies, however, have not yet been done.
Prevention:
Vaccine development
There is no commercially available vaccine for the dengue flavivirus. However, one of the many ongoing vaccine development programs is the Pediatric Dengue Vaccine Initiative which was set up in 2003 with the aim of accelerating the development and introduction of dengue vaccine(s) that are affordable and accessible to poor children in endemic countries. Thai researchers are testing a dengue fever vaccine on 3,000–5,000 human volunteers after having successfully conducted tests on animals and a small group of human volunteers. A number of other vaccine candidates are entering phase I or II testing.
Mosquito control
A field technician looking for larvae in standing water containers during the 1965 Aedes aegypti eradication program in Miami, Florida. In the 1960s, a major effort was made to eradicate the principal urban vector mosquito of dengue and yellow fever viruses, Aedes aegypti, from southeast United States. Courtesy: Centers for Disease Control and Prevention Public Health Image Library
A field technician looking for larvae in standing water containers during the 1965 Aedes aegypti eradication program in Miami, Florida. In the 1960s, a major effort was made to eradicate the principal urban vector mosquito of dengue and yellow fever viruses, Aedes aegypti, from southeast United States. Courtesy: Centers for Disease Control and Prevention Public Health Image Library
Primary prevention of dengue mainly resides in mosquito control. There are two primary methods: larval control and adult mosquito control. In urban areas, Aedes mosquitos breed on water collections in artificial containers such as plastic cups, used tires, broken bottles, flower pots, etc. Continued and sustained artificial container reduction or periodic draining of artificial containers is the most effective way of reducing the larva and thereby the aedes mosquito load in the community. For reducing the adult mosquito load, fogging with insecticide is somewhat effective.
Prevention of mosquito bites is another way of preventing disease. This can be achieved either by personal protection or by using mosquito nets. In 1998, scientists from the Queensland Institute of Research in Australia and Vietnam’s Ministry of Health introduced a scheme that encouraged children to place a water bug, the crustacean Mesocyclops, in water tanks and discarded containers where the Aedes aegypti mosquito was known to thrive. This method is viewed as being more cost-effective and more environmentally friendly than pesticides, though not as effective, and requires the ongoing participation of the community.
Personal protection
Personal prevention consists of the use of mosquito nets, repellents containing NNDB or DEET, covering exposed skin, use of DEET-impregnated bednets, and avoiding endemic areas.
Dengue is caused by the bites of the tiger striped Aedes aegypti mosquito, which, unfortunately, is a daytime mosquito. It hides in dark corners in houses and breeds in clean water in flowerpots and even bottle caps. Also, there is no immunisation as yet against dengue.
One could make sure there is no stagnant water in his or her house. The house should be “mosquito proofed” with mesh covered windows and doors. Wear protective clothing and apply mosquito repellent ointment or liquid on the clothes. The vapourising mosquito repellents will drive away the mosquitoes, but the smoke is toxic to humans also.
Potential antiviral approaches
In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.
The yellow fever vaccine (YF-17D) is a related Flavivirus,[clarify] thus the chimeric replacement of yellow fever vaccine with dengue has been often suggested[clarify] but no full scale studies have been conducted to date.
In 2006, a group of Argentine scientists discovered the molecular replication mechanism of the virus, which could be attacked by disruption of the polymerase’s work
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
