Tag Archives: Aedes aegypti

Zica Virus

Definition:
Zika virus is a member of the virus family Flaviviridae and the genus Flavivirus, transmitted by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus, the same type of mosquito that spreads dengue, chikungunya and yellow fever. The Pan American Health Organization (PAHO) said Aedes mosquitoes are found in all countries in the Americas except Canada and continental Chile, and the virus will likely reach all countries and territories of the region where Aedes mosquitoes are found.
The infection, known as Zika fever, often causes no or only mild symptoms. Since the 1950s it has been known to occur within a narrow equatorial belt from Africa to Asia. In 2014, the virus spread eastward across the Pacific Ocean to French Polynesia, then to Easter Island and in 2015 to Mexico, Central America, the Caribbean, and South America, where the Zika outbreak has reached pandemic levels.

Click  & see  : zika virus – News Images

The Zika virus is found in tropical locales with large mosquito populations. Outbreaks of Zika virus disease have been recorded in Africa, the Americas, Southern Asia and the Western Pacific. The virus was first identified in Uganda in 1947 in rhesus monkeys and was first identified in people in 1952 in Uganda and Tanzania, according to the World Health Organization.
Transmission:
The vertebrate hosts of the virus were primarily monkeys in a so-called enzootic mosquito-monkey-mosquito cycle, with only occasional transmission to humans. Before the current pandemic began in 2007, Zika virus “rarely caused recognized ‘spillover’ infections in humans, even in highly enzootic areas”. Infrequently, other arboviruses have become established as a human disease though, and spread in a mosquito–human–mosquito cycle, like the yellow fever virus and the dengue fever virus (both flaviruses), and the chikungunya virus (a togavirus)

Can Zika be transmitted through sexual contact?

Two cases of possible person-to-person sexual transmission has been described, but the PAHO said more evidence is needed to confirm whether sexual contact is a means of Zika transmission.

It is unknown whether women can transmit Zika virus to their sexual partners. As of February 2016, the CDC recommends that men “who reside in or have traveled to an area of active Zika virus transmission who have a pregnant partner should abstain from sexual activity or consistently and correctly use condoms during sex (i.e., vaginal intercourse, anal intercourse, or fellatio) for the duration of the pregnancy.” Men who reside in or have traveled to an area of active Zika virus transmission and their non-pregnant sex partners “might consider” abstinence or condom use. The CDC did not specify how long these practices should be followed with non-pregnant partners because the “incidence and duration of shedding in the male genitourinary tract is limited to one case report” and that “testing of men for the purpose of assessing risk for sexual transmission is not recommended.

The PAHO also said Zika can be transmitted through blood, but this is an infrequent transmission mechanism. There is no evidence the virus can be transmitted to babies through breast milk.

CDC issued new recommendations to those who have traveled to Zika-prone areas: Use condoms during sex or don’t have sex. – Click  & See 
Symptoms:
Zika virus is related to dengue, yellow fever, Japanese encephalitis, and West Nile viruses. The illness it causes is similar to a mild form of dengue fever, is treated by rest, and cannot yet be prevented by drugs or vaccines. There is a possible link between Zika fever and microcephaly in newborn babies by mother-to-child transmission, as well as a stronger one with neurologic conditions in infected adults, including cases of Guillain–Barré syndrome.

People who get Zika virus disease typically have a mild fever, skin rash, conjunctivitis, muscle and joint pain and fatigue that can last for two to seven days. But as many as 80 percent of people infected never develop symptoms. The symptoms are similar to those of dengue or chikungunya, which are transmitted by the same type of mosquito.

Diagnosis:
The PAHO said there is no evidence that Zika can cause death, but some cases have been reported with more serious complications in patients with pre-existing medical conditions.

The virus has been linked to microcephaly, a condition in newborns marked by abnormally small heads and brains that have not developed properly. It also has been associated with Guillain-Barre syndrome, a rare disorder in which the body’s immune system attacks part of the nervous system. Scientists are studying whether there is a causal link between Zika and these two disorders.

Treatment:
There is no defenite treatment developed yet.Patients are adviced to take rest. Doctors sometimes prescribe few nominal medicines to get little relieve from extenal symptoms.

Prevention:
Defense against mosquitoes is defense against Zika. The CDC recommends long clothing and insect repellent. If you develop symptoms, go see a doctor.

Vaccine development:
Effective vaccines exist for several flaviviruses. Vaccines for yellow fever virus, Japanese encephalitis, and tick-borne encephalitis were introduced in the 1930s, while the vaccine for dengue fever only became available for use in the mid-2010s.

Work has begun towards developing a vaccine for Zika virus, according to Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases.  The researchers at the Vaccine Research Center have extensive experience from working with vaccines for other viruses such as West Nile virus, chikungunya virus, and dengue fever.   Nikos Vasilakis of the Center for Biodefense and Emerging Infectious Diseases predicted that it may take two years to develop a vaccine, but 10 to 12 years may be needed before an effective Zika virus vaccine is approved by regulators for public use.

Indian company Bharat Biotech is working on two approaches to a vaccine: “recombinant”, involving genetic engineering, and “inactivated”, where the virus is incapable of reproducing itself but can still trigger an immune response. On 3 February 2016, the company claimed animal trials of the inactivated version would commence in two weeks.

Since April 2015, a large, ongoing outbreak of Zika virus that began in Brazil has spread to much of South and Central America and the Caribbean. In January 2016, the CDC issued a level 2 travel alert for people traveling to regions and certain countries where Zika virus transmission is ongoing.   The agency also suggested that women thinking about becoming pregnant should consult with their physicians before traveling. Governments or health agencies of the United Kingdom, Ireland, New Zealand,   Canada, and the European Union soon issued similar travel warnings. In Colombia, Minister of Health and Social Protection Alejandro Gaviria Uribe recommended to avoid pregnancy for eight months, while the countries of Ecuador, El Salvador, and Jamaica have issued similar warnings.

Plans were announced by the authorities in Rio de Janeiro, Brazil, to try to prevent the spread of the Zika virus during the 2016 Summer Olympic Games in that city.

According to the CDC, Brazilian health authorities reported more than 3,500 microcephaly cases between October 2015 and January 2016. Some of the affected infants have had a severe type of microcephaly and some have died. The full spectrum of outcomes that might be associated with infection during pregnancy and the factors that might increase risk to the fetus are not yet fully understood. More studies are planned to learn more about the risks of Zika virus infection during pregnancy. In the worst affected region of Brazil, approximately 1 percent of newborns are suspected of being microcephalic.

Click & see  : 2007 Yap Islands Zika virus outbreak   
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:
https://en.wikipedia.org/wiki/Zika_virus
http://www.whio.com/news/news/national/what-zika-virus-and-isnt/nqKzc/
http://news.yahoo.com/factbox-why-zika-virus-causing-alarm-233408770.html;_ylt=AwrXnCHbw7ZWumkA6oHQtDMD;_ylu=X3oDMTByNDZ0aWFxBGNvbG8DZ3ExBHBvcwM2BHZ0aWQDBHNlYwNzcg–

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Stop Dengue in its Tracks

Dengue fever is caused by the Aedes egypti mosquito. Culex and Anophelesmosquitoes (which cause diseases like malaria and filaria) are nocturnal — that is, they emerge and bite at night. They can be effectively kept at bay by using mosquito nets while sleeping at night. Aedes egypti, however, is a daytime urban insect. It cannot live above 1,220m or fly more than a hundred metres. It is easily identifiable — its body is striped like that of a tiger. It lives in houses and breeds in stagnant water. This could be in flower vases, old tyres, upturned bottle caps, and even water that collects on leaves and plants.

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Eradication of their breeding grounds is, therefore, a Herculean task, which cannot be achieved by the government alone. Citizens need to do their bit, awaken their civic sense and keep their neighbourhood garbage free. At home, flower vases, water cooler trays, and all sorts of open containers — including broken mugs and bottle caps — should be emptied.

The government often uses frogs or sprays of insecticides to reduce the population of Aedes egypti in populated areas. The sprays need to be used every eight to 10 days to interrupt the cycle of virus transmission. Also, people must leave their doors and windows open so that the insecticide can penetrate indoors, into the nooks and crannies where the mosquitoes rest. We often close all openings to prevent the “harmful chemicals” from entering inside. This negates the effects of spraying.

Once an infected mosquito bites, there is an asymptomatic incubation period of five to six days. After this, dengue sets in abruptly with headache and high fever. There is pain behind the eyes and on moving the eyes. Severe body ache makes it difficult for the person to move, giving dengue the nickname “back breaking” fever. There may be rashes on the skin and inside the mouth. There may also be bleeding into the conjunctiva of the eyes, making them appear blood shot.

After three or four days, the temperature returns to normal. But this is only a temporary respite; the fever returns a few days later with all the previous symptoms but in a milder form. Dengue is, therefore, also called “saddle back” fever.

Unfortunately, there is no specific treatment for dengue. There is no vaccination (as yet) to prevent infection or specific antiviral medication to combat the condition. Affected persons have to ride out the disease with supportive treatment, hoping for the best. Treatment is symptomatic with paracetamol for lowering the fever and fluids for hydration. Aspirin and non-steroidal anti-inflammatory agents like brufen must be avoided. Blood transfusions may have to be given if there is bleeding and shock.

The first attack of dengue usually takes a few weeks to completely recover from. Overall, the disease has a five per cent mortality. It is especially dangerous in children. The dangerous form, called dengue haemorrhagic fever, which is accompanied by shock and bleeding, occurs with subsequent infections with the virus, especially if they are of a different “serotype”.

Humans are infective during the first three days when the virus is multiplying in the blood. During this period, it’s important they lie inside a mosquito net all day and night. This is to prevent them from infecting other members of the household.

The diagnosis is made by excluding other causes of fever. Blood tests may show a low white cell count and platelets. There are, however, some confirmatory tests, like complement fixation, Elisa and an increasing number of antibodies.

Dengue is a self-limited disease. The severity of the symptoms depends on the serotype of the virus, immunological status of the host and, to some extent, genetics.

Herbal products — such as fresh leaves and extracts of neem and tulasi — are being investigated for their anti viral and immune boosting properties. The results are not conclusive. Claims and counterclaims about the efficacy of herbal products are difficult to evaluate. Double blind control studies have not yet been done to prove or disprove their efficacy.

One can prevent mosquito bites to a certain extent by wearing long-sleeved clothing, sleeping inside a mosquito net, and using mosquito meshes for windows and doors. Water should not be allowed to stagnate in containers in and around residential areas. Adding a handful of rock salt or pouring kerosene into stagnant water prevents mosquitoes from breeding.

Remember, no vaccine or specific treatment exists — the only way to escape dengue is to prevent being stung by these pesky insects.

Source: The Telegraph (Kolkata, India)

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Curare

 

Botanical Name: Chondrodendron tomentosum
Family:Menispermaceae
Genus: Chondrodendron
Species: Tomentosum
Parts Used: Leaf, Root

Synonyms: Pereira Brava. Cissampelos Pareira. Velvet Leaf. Ice Vine.
Parts Used: Dried root, bark, bruised leaves.

Common Names: Curare, Grieswurzel, Pareira Brava, Pareira, Vigne Sauvage,  pareira, uva-da-serra, uva-do-mato, ampihuasca blanca, antinupa, antinoopa, comida de venados, curari, ourari, woorari, worali, velvet leaf

Habitat: Curare is native to   West Indies, Spanish Main Brazil, Peru.  It grows in  Amazon Basin of South America.(In El Salvador and other parts of Central America)

Description:
This deciduous plant will flower in a container just prior to leafing out. The flowers are attractive red “spikes”. Zone 9+ The bright red seeds contain a number of poisonous alkaloids that have a curare-like action.

CLICK TO SEE THE PICTURES

Curare grows as a large liana, or vine, found in the canopy of the South American rainforest. The vine may get as thick as 4 inches in diameter at its base. It has large alternate, heart-shaped leaves which may be 4-8 inches long and almost as wide, with a 2-6 inches long petiole. The leaves are smooth on top with a hairy white bottom, and deeply indented veins radiating from the leaf base. Clusters of small (1/16-1/8 inches), greenish-white flowers are made up of separate male and female flowers. The fleshy fruits are oval, narrow at the base, and approximately 1-2 mm long.

Edible Uses:

The fruit of this vine is edible with a bitter-sweet taste.
Some Indians of South America crush and cook the roots and stems, and add other plants and venomous animals, mixing it until it becomes a light syrup. They call this mixture “ampi”, or “curaré”, which they use on the tip of their arrows and darts to hunt wild game. Crude curare is a dark brown or black mass with a sticky to hard consistency and an aromatic, tarry odor. The name comes from Indian word meaning “poison.”

Curare, in large doses, paralyses the motor nerve-endings in striped muscle, and death occurs from respiratory failure. Curare is very bitter, and is actually a common name for various dart poisons originating from South America.

The young flowers and new growth are added to soups and other food preparations as a soporific vegetables.

Curare has differing effects depending upon dosage, whether it is injected into muscle tissue, or ingested. Curare is used internally in tribal medicine for edema, fever, kidney stones and testicular inflammation. It is also known to relax muscles into a state of inactivity.

Under appropriate medical care and attention, curare is also used to relieve spastic paralysis, to treat some mental disorders, and to induce muscle relaxation for setting fractures. Curare is now used extensively in modern medicine. It is only toxic if it enters the bloodstream. Curare is not for sale to the general public.

As with many Amazonian tribal plant history and legend, curare is prepared by old women. In some traditions, the witch doctor has a monopoly of the business, but generally, wise old men get together to brew a batch. Extra curare was usually carried by tribal members in a gourd or calabash, and stored with weapons.

Medicinal Uses:

The active ingredient in “curaré”, D-tubocurarine, is used in medicine. Brazilians consider the root a diuretic, and use it internally in small quantities for madness and dropsy, and externally for bruises. It is also used for edema, fever, and kidney stones.

Curare is an alkaloid, and acts as a neuromuscular blocking agent to produce paralysis in muscles. It first affects the muscles of the toes, ears, and eyes, then those of the neck, arms and legs, and finally, those involved in breathing. In fatal doses, death is caused by respiratory paralysis. Curare must get into the blood system for it to work. It doesn’t hurt to eat something killed by a poisoned curare arrow, for instance.

The therapeutical employment of curare has been suggested in certain severe and obstinate spasmodic affections, as in epilepsy, chorea, hydrophobia, and, more particularly, in tetanus. It is used by subcutaneous injections of its filtered aqueous solution, thus: Add curare 1 grain, to distilled water 24 minims; dissolve, let the solution stand 48 hours, and filter; of this, from 2 minims (1/12 grain) to 6 minims (1/4 grain) may be used at one injection, carefully repeating the injections until relaxation of the muscles has been effected. Curarine, dissolved in water, with a few drops of sulphuric acid added, to facilitate its solution, is to be used in still smaller doses—from the 1/240 to the 1/120 part of a grain. It is doubtful whether this agent will ever come into general use as a medicinal remedy; at least, not so long as other medicines are known in which greater confidence can be placed. The diversity of action, attributable, in some instances, to its difference of composition, in others to its inertness, or to its highly active qualities, render it an uncertain, as well as an unsafe, remedy.

It is used in modern medicine primarily as an auxiliary in general anesthesia, frequently with cyclopropane, especially in abdominal surgery. Upon injection, curare acts as a neuromuscular blocking agent to produce flaccidity in striated (striped) muscle (it competes with acetylcholine at the nerve ending, preventing nerve impulses from activating skeletal, or voluntary, muscles). It first affects the muscles of the toes, ears, and eyes, then those of the neck and limbs, and, finally, those involved in respiration. In fatal doses, death is caused by respiratory paralysis.
Practitioners commonly rely on velvet leaf as an excellent natural remedy for menstrual difficulties, including cramping and pain, premenstrual syndrome (PMS), excessive bleeding, and fibroid tumors. Its ability to curb excessive menstrual bleeding very quickly can be quite remarkable. It is often employed in overall female balancing formulas, in kidney formulas (for its diuretic and smooth-muscle relaxant effects), and, in combination with other plants, in heart tonics and hypertension remedies. It is also considered effective against malaria, fever, hepatic ailments, gastric ulcers, diabetes, anemia, high cholesterol, cerebral tonic, fever, typhoid, stomach ulcers, pain killer, chronic inflammation of the urinary passages, good diuretic, etc. In North American herbal medicine, velvet leaf is used for many of the same conditions as in South America as well as for inflammation of the testicles and minor kidney problems. Pereira root also acts as an antiseptic to the bladder and is therefore employed for the relief of chronic inflammation of the urinary passages. It is also a good diuretic. The decoction of the stems and roots mixed with wild bee honey is used to treat sterile women. Root decoction used for post-menstrual hemorrhages, the alcoholic maceration, for rheumatism. Macerated leaves, bark and root, mixed with rum, are used by as aphrodisiac. Root decoction used as a cardio tonic, anti-anemic, anti-malarial. One tribe use a leaf decoction for fever and another use the decoction of the bark and stem as a dental analgesic. Some Ecuadorian tribes use the leaf decoction for conjunctivitis and snakebite. Others use the root tea for difficult delivery and nervous or weak children with colic. Also used in homeopathy, in the form of a mother tincture.

Abutua is a very useful herb for women’s affections. Its antispasmodic action makes it influential in treating cramps, painful menstruation and pre and post-natal pain. Brazilian Indian women have for centuries valued its analgesic powers, and the satchels of almost all midwives contain the root of this plant. Helpful for menstrual cramps and difficult menstruation, pre- and post-natal pain Aids poor digestion, drowsiness after meals and constipation.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://www.blueplanetbiomes.org/curare.htm
http://ezinearticles.com/?Rainforest-Plants—Curare&id=1030007
http://www.britannica.com/EBchecked/topic/146779/curare

http://www.henriettesherbal.com/eclectic/kings/curare.html

http://www.herbnet.com/Herb%20Uses_UZ.htm

 

Yellow Fever

TEM micrograph: Multiple yellow fever virions ...

Image via Wikipedia

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.

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pictures

Sylvatic yellow fever (monkey to human)

* 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.

……………You may click to see pictures of  mosquitoes  causing yellow fever.….

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.

Symptoms :-
*Arrhythmias, heart dysfunction
*Bleeding (may progress to hemorrhage)
*Coma
*Decreased urination
*Delirium
*Fever
*Headache
*Jaundice
*Muscle aches (myalgia)
*Red eyes, face, tongue
*Seizures
*Vomiting
*Vomiting blood

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.

CLICK TO READ ..>: Early sign of yellow fever could lead to new treatment

Prognosis: :-

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

Possible Complications :-

*Coma
*Death
*Disseminated intravascular coagulation (DIC)
*Kidney failure
*Liver failure
*Parotitis
*Secondary bacterial infections
*Shock

Prevention :-

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.

click to see the picture

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

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Dengue Fever

Definition:

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.

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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.

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Aedes aegypti mosquito

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.

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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. 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

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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.

Resources:
http://en.wikipedia.org/wiki/Dengue_fever
http://www.medicinenet.com/dengue_fever/article.htm#1whatis

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