- ATTENTION -



FELLOW BALD MEN AND MEN JUST STARTING TO GO BALD or WOMEN LOSING THEIR HAIR
CURRENT TREATMENT METHODS DO NOT WORK...BECAUSE WHAT WE HAVE BEEN TOLD UNTIL NOW IS NOT COMPLETELY TRUE!!!
DHT (dihydrotestosterone) IS NOT THE MAIN genetic CAUSE OF HAIR LOSS
LEARN ABOUT THE REAL GENETIC CAUSE OF HAIR LOSS AND HOW TO TREAT IT
STOP HAIR LOSS NOW, GROW NEW HAIR AND THICKEN THIN HAIR WITH A SIMPLE NEW TREATMENT METHOD BASED ON A RADICAL "NEW" THEORY ABOUT THE TRUE GENETIC CAUSE OF HAIR LOSS BUT WHICH USES AN OLD "ESTABLISHED" ELECTRICAL SCIENCE TO STIMULATE THE FOLLICLES.

NO DRUGS...NO LOTIONS...NO SURGERY
IT'S THE ALL NEW
"Maliniak Method"
FROM
BORN AGAIN
-The ALTERNATIVE SCIENCE company-
By LEON MALINIAK, B.A., B.C.L.
There are many hair loss treatments out there including transplant surgery, laser lamps, massage and drugs such asPropecia and Rogaine. They all work to a degree but none of them provides very satisfactory results and none of them has grown new hair on a COMPLETELY bald scalp...
 ...that's because they do not treat the true genetic cause of hair loss.

The conventional wisdom is that hair loss is caused by 5 Alpha-Reductase which converts ordinary testosterone into DHT (dihydrotestosterone). DHT gets into the follicles and puts them into a dormant state until they eventually stop producing hair. I always knew it could not be the only cause of hair loss because no man goes bald on the SIDES or BACK of the scalp, but only on TOP. These different areas are all exposed to DHT, so it made no sense that DHT was the only explanation. I knew there had to be some other UNKNOWN factor at work, so I started doing research on this problem again from scratch.

I was surprised to discover something about the anatomy of the scalp which I had never seen before even though I have been studying hair loss for thirty years. As soon as I saw it, I knew this was the MISSING PIECE of the puzzle. It's the third layer of skin at the TOP of the scalp and it's called the GALEA APONEUROTICA.
This GALEA is a tendon-like tissue which exists ONLY on the TOP of the scalp. It almost looks like a helmet and its shape matches exactly the worst cases of male pattern baldness. This GALEA is attached to muscles all around the head which PULL on it and STRETCH it in all directions. That's why all bald guys look like they have a stretched, SHINY scalp. This "chokes" off the blood flow. 
We only go bald in those areas where this GALEA exists and nowhere else on the scalp.
I did not invent the idea that this GALEA may be involved in hair loss, it's been debated for years and it is still being debated. I finally realised that this endless debate was not resulting in any action being taken so I took a stand and decided that from the preponderance of all of the evidence and on a balance of probabilities, that it is more logical to conclude that  this GALEA is in fact involved in hair loss and male pattern baldness and decided to do something about it.


But since all men have a GALEA and yet not all men lose their hair or get male pattern baldness, I concluded that it isonly in those men who have a genetic pre-disposition to developing an extremely tight GALEA, or where it becomesvery tight due to extreme STRESS, where this GALEA is a factor in hair loss.

I  then incorporated it into a comprehensive NEW THEORY that says hair loss is caused by TWO things and not just one; firstly, by a tight GALEA, which blocks blood flow and nutrients to the follicles AND then secondly, by DHTwhich accumulates in the follicles, due to this disrupted blood flow, making them dormant and unable to grow new hair. Newly released scientific studies, which I refer to below, now suggest that there is also an "overproduction" of DHT when levels of OXYGEN are reduced, which is again consistent with my view about the role of the GALEA disrupting blood flow and which would explain this reduced oxygen level.

This "completes the circle" and suggests that the disrupted blood flow from the tight GALEA results in both anaccumulation and overproduction of DHT in the follicles and it is now even more logical to conclude that it is all this extra DHT which then causes the hair loss and male pattern baldness only in those areas where this GALEA exists and nowhere else and only in those people whose GALEA is very stretched and tight.

The exact mechanism by which the DHT causes it's damage is not fully understood but there is still no doubt that it is the actual "killer" of follicles, as the conventional wisdom states. What's never been properly explained until now isWHY the DHT does this in why it only happens in some people and not others. Every man has DHT, so why isn't every male bald? Women also have a GALEA, so why do most woman not lose their hair?

The MALINIAK METHOD finally answers these questions with this new TWO FACTOR THEORY of hair loss by saying the DHT becomes a problem only in those men who FIRSTLY, have this tightened GALEA,  which chokes off the blood supply, allowing DHT to accumulate and as  these recent scientific studies suggest, cause DHT to beoverproduced due to the lower oxygen levels. Those few women who eventually lose their hair or have hair loss, even though they may have had a tight GALEA for years, only do so if  they develop the second problem at some point in life, as only some of them do, which is the elevated levels of DHT due to menopause or childbirth.
MORE IMPORTANTLY, I developed a NEW METHOD to stimulate dormant follicles and grew NEW HAIR on areas which were bald for years...contrary to everything we have told till now.
THE NEW TREATMENT METHOD
Based on this new theory, the treatment method first relaxes this GALEA with massage and then uses a special electrical device to stimulate the follicles into growing hair again. (It isnot a laser comb). 
The device we use is based on an old established science which is still used today but for other purposes. I chose it because unlike other devices, it deeply vibrates the hair follicle. My theory is that this vibration does two things; firstly it "dislodges" the trapped DHT and secondly, it stimulates the hair growing machinery in the follicles to work normally again. The follicles wake up from their dormant state and "REBOOT". They act like normal follicles and once again GROW NEW HAIR. This also STOPS continued excessive hair loss and THICKENS THIN HAIR.
The "MALINIAK" method:  NO DRUGS, NO LOTIONS and NO SURGERY.
THE LATEST SCIENTIFIC NEWS NOW CONFIRMS OUR THEORY
This website was first activated about one year ago. Now, recent new scientific studies have confirmed the validity of the TWO main premises of the "MALINIAK METHOD" which we suggested one year ago and also contribute other explanations of WHY our suggested treatment techniques work.
Firstly, a study by Brian J.Freund at the Crown Institute in Pickering, Ontario published in the "Journal of Plastic and Reconstructive Surgery" used botoxin to relax the GALEA and thereby triggered some new hair growth, concluding that a tight GALEA is in fact involved in hair loss as is suggested by the MALINIAK METHOD. It also concluded that the restricted blood flow interfered with the production of oxygen and this lower level of oxygen caused an overproduction of DHT.
This supports and proves the first hypothesis of the "MALINIAK METHOD" that the GALEA is in fact involved in hair loss. It may also explain another reason why the electrical stimulator we use, which does several other things, but which also generates oxygen, is able to revive dormant follicles by also restoring the normal levels of DHT production. This effect would be in addition to the other ways our electrical device stimulates the follicles which includes high frequency "vibration" of the follicles at a cellular level, which we theorize both REVIVES the dormant follicles and also dislodges what we now  know is this "overproduced" DHT as well as helping to "dislodge" the already accumulated DHT, according to our theory.
However, this botoxin approach ALONE does not stimulate very significant hair growth which we would explain by saying that it's because, according to our theory, it only addresses "one-half" of the problem. The MALINIAK METHOD, states that  HAIR LOSS and Male Pattern Baldness is caused by TWO FACTORS,  and therefore treats both the first and second parts of the problem, the tight GALEA and the DHT accumulation and more importantly, provides a new idea and method to stimulate the dormant follicles to become active again by reviving an "old established" science.
This botoxin approach also uses a controversial and potentially dangerous drug to relax the GALEA and our system does not need, nor does it encourage or tolerate the use of any drugs.
NO DRUGS, NO LOTIONS, NO SURGERY.
The second study was conducted at the University of Pennsylvania by George Cotsarelis and published in the Journal of Clinical Investigation. It found that bald areas and non-bald areas have the same number of "stem cells" but the non-bald areas had more "progenitor" cells, which are a more mature form of the stem cells. It concluded that these stem cells could in fact be stimulated to transform into these "progenitor cells" and grow hair again in bald areas. Therefore, contrary to the previous conventional wisdom, "dormant" follicles can in fact be revived, as originally suggested by the MALINIAK METHOD one year ago, and more importantly, we actually have a treatment method by which to do this using our electrical stimulator. This study therefore confirms the second premise of the MALINIAK METHOD that "dormant" follicles can in fact be rejuvenated to grow hair again".
All of this represents "independant scientific" proof and validation of the TWO main underlying premises of the MALINIAK METHOD predicted one year ago.
WOMEN'S HAIR LOSS
WOMEN also have a GALEA and it is LOGICAL to conclude that it can also get tight. But based on this new TWO factor theory about the cause of hair loss, I concluded that most women do not lose their hair even if they have a tight GALEA because the majority of women do NOT have the second problem, which is elevated levels of testosterone or its by product DHT.
But many women do experience changes in their hormone levels at some point in their lives and this causes them all kinds of health problems. For such women, if they lose their hair or their hair becomes THIN, and it is NOT otherwise due to ILLNESS or CHEMOTHERAPY, then it is logical to conclude that it is also due to the combined effects of this tight GALEA and their NEWLY elevated levels of testosterone or DHT, in the same way as in causes hair loss in men.
Based on this analysis, it is also logical to conclude that this new treatment method would also work for women, and perhaps that it would work even better than for men because women have not had the built-up or negative effects ofDHT for as long as most men with this problem.
THE RESULTS SO FAR
I had used the system on myself for only about four months and yet the results were so remarkable that a close friend of mine, BERNARD GURBERG, owner of DOLLAR CINEMA in Montreal, insisted that I make this system available to other people. I first wanted to be sure that my results were stable and that I continued to grow new hair.

It soon became obvious that not only did this method STOP my HAIR LOSS but my NEW HAIR growth wascontinuing and accelerating, first in areas which had gone bald in the last few years and then in areas where I havebeen bald for thirty (30) years!
Leon January 2010 - Before using the Maliniak Method
April 2010 - 3 months using the Maliniak Method
June 2010 - 5 months using the Maliniak Method
June 2010 - 5 months using the Maliniak Method
August 2010 - 7 months using the Maliniak Method
August 2010 - 7 months using the Maliniak Method
November 2010 - 10 months using the Maliniak Method
December 2010 - 11 months using the Maliniak Method
December 2010 - 11 months using the Maliniak Method
December 2010 - 11 months using the Maliniak Method
I do not want to exaggerate because I just started this program and my hair is still thin but there is no doubt that my HAIR LOSS has stopped and new hair is definitely growing everywhere. I knew it would take patience because follicles which have been dormant for a long time will not revive overnight but I stuck with it and it worked.

I am 61 years old and I have been bald for years but this method started working EVEN for me and results showed up very quickly. If my hair continues to grow at this pace, GOD WILLING, I will have a full looking head of new hairwithin ONE year.

I even realize and accept that at my age I may never get back all my hair or that it may never look like a really full head of hair, but for someone who has been bald for years, what I have already recovered is a MIRACLE and I no longer feel bald or helpless against this problem.
FOR YOUNGER MEN, THIS METHOD SHOULD WORK FASTER ANDBETTER  BECAUSE THEIR FOLLICLES HAVE NOT BEEN DORMANT FOR AS LONG AND ARE NOT AS CLOGGED WITH DHT AS WITH OLDER MEN.
These results have now been replicated in at least six "informal" test subjects of different ages, where the younger guys, aged 21 and 24, stopped their hair loss within three to four weeks and they started growing new hair. I myself didn't even believe that at first, but when I thought about it I realized that if this theory is really valid and true, then if the PROCESS causing the hair loss is stopped...it is logical that in these younger men their hair would stop falling out almost immediately and their hair would start to grow again.
TESTIMONIALS FROM 3 OF OUR CUSTOMERS
These claims will not impress the mainstream medical community who insist on the standard scientific criteria of  "peer-reviewed, double-blind studies with placebos and control groups" but I submit that the theory is fundamentally LOGICAL and there is sufficient anecdotal and quasi-scientific evidence to validate the theory and the effectiveness of the MALINIAK METHOD. Since the medical community has failed to cure baldness with their conventional approach till now I am not afraid to propose this new theory and I challenge any of them or any other sceptic to try to get these same results and grow new hair on a previously bald scalp by just "telling" people they are getting the treatment, which is the essence of the PLACEBO effect...NO WAY!

Some of you will obviously be sceptical and will want to wait for more results, so don't buy the book now.

However, for those of you who like the "LAYMAN'S LOGIC" of this theory and think the reasoning behind the treatment method makes sense, then become a part of this process of discovery and exploration and start right now.
HOW LONG DOES IT TAKE?
The MALINIAK METHOD only takes about thirty (30) minutes per day and it is very simple.
YOUNGER MEN will have to do it every day to start but after a few months, once the hair has stopped falling and new hair has started to grow they should be able to maintain the progress by just doing it two or three times a week. After about one year they will theoretically only need to do it once a week, but results will vary.
OLDER men who have been bald for a long time will most probably take longer to get initial results, like in my personal case, and will have to stay with it longer to maintain their gains and keep growing hair. But, I know that any man in this position will be glad to make this small sacrifice if he gets his hair back. I think of it as a daily personal grooming function, like BRUSHING MY TEETH.
I invite you to order our e-booklet and start using this system immediately. Come along for the ride.
This method has been conceived and developed for use only in cases of normal hair loss and MPB and is NOT effective for hair loss due to CHEMOTHERAPY or some other underlying medical condition.
Here's how to order the MALINIAK METHOD
from BORN AGAIN right now for only $29.95
  
* You can start using the Method even before you have purchased the equipment.
* You don't need a PayPal account. You can pay with your credit card.
* You only need to purchase the equipment ONCE.
* Your Order is Secure and Fully Guarateed by PayPal.
* Your Credit Card will show a charge by PayPal.
* After your credit card has been approved, you will be taken to a special download page where you can download:
STOP HAIR LOSS and GROW NEW HAIR with the "MALINIAK METHOD" immediately.
* You will also receive an email with a download link. You will have 24 hours to download the file.
* Your eBook will be an Adobe pdf file in ENGLISH.
* The pdf file will be 4.31 MB and will take about 14 seconds to download on a 3 MB/sec connection.
* You will need Adobe Reader to view the eBook on you PC or Mac.
DOWNLOAD IT AND GET THIS PROGRAM RIGHT NOW and YOU WILL RECIEVE
* 2  instructional videos demonstrating 2 critical techniques.
* Maliniak Method Quick Start Guide - to get you started instantly.
* FREE revisions of the Maliniak Method.
* An easy to understand booklet telling you the THREE EASY STEPS to follow with this system and a detailed explanation of the science and thinking behind it so you can see for yourself how logical it is.
* We will tell you the name of the special electrical stimulation devicewhich you can buy yourself directly from many suppliers for prices starting at $79.00 
* It has NOTHING TO DO WITH LASERS LAMPS and although this electrical stimulator is an important part of the system, you will NOT get any significant new hair growth with this device alone. You must follow the other steps of the system.
* You will also receive a supplementary section with my analysis and review of the whole field of ALTERNATIVE or COMPLIMENTARY medicine which I have researched and studied for YEARS. It will tell you about my CONCLUSION for what seems to be the SIMPLEST, MOST LOGICAL and EFFECTIVE type of ALTERNATIVE APPROACH TO MEDICAL TREATMENT which should be tried BEFORE drugs, surgery or radiation.
I personally understand the tremendous emotional pain of HAIR LOSS and the added frustration of not being able to do anything about it. I had a constant feeling of being "helpless"...BUT NOT ANY MORE.
HOW MUCH DOES IT ALL COST?
THE BEST THING ABOUT THE MALINIAK METHOD IS THAT IT IS SIMPLE AND IT IS NOT EXPENSIVE COMPARED TO ANY OTHER HAIR LOSS TREATMENT.

YOU MAKE A "ONE TIME" PURCHASE TO BUY THE BOOK FOR $29.95 AND YOU WILL GET FREE UPDATES;

YOU MAKE A "ONE TIME" PURCHASE TO BUY THE ELECTRICAL STIMULATOR. IT CAN BE FOUND ON THE POPULAR SITE   FOR LESS THAN $100.00. THE LINKS ARE ALL FOUND IN THE EBOOK. 
THERE ARE NO CONTINUOUS MONTHLY EXPENDITURES LIKE WITH DRUGS OR LOTIONS OR SURGERY WHICH END UP COSTING THOUSANDS AND THOUSANDS OF DOLLARS.
M y HAIR is now BORN AGAIN and that's how I feel too.
BACKGROUND INFO ABOUT THE INVENTOR OF THE "MALINIAK" METHOD
My name is LEON MALINIAK, B.A., B.C.L., and I am a McGill University Law School graduate. My undergrad degree, also from McGill, was in Psychology. I have been doing medical research for many years because of two bouts of cancer in my family. My daughter contracted leukemia in 1990 when she was three years old. I reviewed 900 medical studies and learned of the existence of a new test based on P.C.R. technology, which greatly improved the "detection of minimal residual disease" and thereby helped children to avoid relapses. It is the same science used to analyze blood at a crime scene. I submitted a written report to a committee of doctors at the Montreal Children's Hospital, they adopted my proposal and my daughter was the first patient they applied it to and she survived, thankGOD. She is now 24 years old and a Cordon Bleu chef.

For the last six years it has been my wife's battle with stage four breast cancer. I was again compelled to do extensive research. I interact with the doctors constantly and also provide her with ALTERNATIVE protocols which I have no doubt have helped her to survive and I will continue to be pro-active until she is completely cured. I will never give up.

I also published a theory for the PREVENTION OF DUCTAL BREAST CANCER which received favourable feedback from a mainstream medical foundation and I am pushing for its implementation.
HOW I STARTED ON THE SUBJECT OF HAIR LOSS AND GROWING NEW HAIR.
I am 61 years old now and I started losing my hair rapidly when I was 18. I went to a type of "hair clinic" which existed at that time knowing in advance that it was probably BALONEY, but I was desperate.

They gave me treatments for a year consisting of scalp massage, pore cleaning, and they also used a machine which was very interesting and it definitely stopped my hair from falling out. I theorized that most of what they were doing was just stimulating the blood circulation in my scalp and cleaning my pores so I continued this myself for years. I believe they helped me get through the "critical" initial phase of elevated testosterone production.

I kept most of my hair until I was 40 years old. It then started to thin slowly but this last year I suddenly realized how bald I was on top. All of my hair had completely fallen out and except for a small patch of hair in front and I now had the classic "crescent" shaped BALD shiny dome.

In a panic, I tried the standard form of massage I had used for years but it did not work. Then I thought about that former "hair clinic" and wondered if the machine they used could help. I did extensive research until I finally found out what that machine was and I bought one. But that also did not help by itself either.

It was only after I opened my eyes to the whole new aspect of this problem about the GALEA that I finally developed a comprehensive new THEORY about hair loss and put together a very simple THREE STEP system which actually stopped my HAIR LOSS and grew "new hair" on my totally bald scalp.

Comments

Post a Comment

Popular Posts

From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Dengue fever (disambiguation). Dengue fever Classification and external resources The typical rash seen in dengue fever ICD-10 A90. ICD-9 061 DiseasesDB 3564 MedlinePlus 001374 eMedicine med/528 MeSH C02.782.417.214 Dengue fever (UK: /ˈdɛŋɡeɪ/, US: /ˈdɛŋɡiː/), also known as breakbone fever, is an infectious tropical disease caused by the dengue virus. Symptoms include fever, headache, muscle and joint pains, and a characteristic morbilliform skin rash. In a small proportion of cases the disease develops to the life-threatening dengue hemorrhagic fever (bleeding, low levels of blood platelets and blood plasma leakage) and dengue shock syndrome (circulatory failure). Dengue is transmitted by several species of mosquito within the Aedes genus, principally A. aegypti. The virus has four different types; infection with one type usually gives lifelong immunity to that type, but only short-term immunity to the others. Subsequent infection with a different type is believed to increase the risk of severe complications. As there is no vaccine, prevention is sought by reducing the habitat and the number of mosquitoes and limiting exposure to bites. Treatment of acute dengue is supportive, using either oral or intravenous rehydration for mild or moderate disease, and intravenous fluids and blood transfusion for more severe cases. The incidence of dengue fever has increased dramatically over the last 50 years, with around 50–100 million people infected yearly. Dengue is currently endemic in more than 110 countries. Early descriptions of the condition date from 1779, and its viral cause and the transmission were elucidated in the early 20th century. Dengue has become a worldwide problem since the Second World War. Contents [hide] 1 Signs and symptoms 1.1 Clinical course 1.2 Associated problems 2 Cause 2.1 Virology 2.2 Transmission 2.3 Predisposition 3 Mechanism 3.1 Viral reproduction 3.2 Severe disease 4 Diagnosis 4.1 General 4.2 Classification 4.3 Virology and serology 5 Prevention 6 Management 7 Epidemiology 8 History 8.1 Etymology 8.2 Discovery 9 Research 10 Notes 11 References 12 External links Signs and symptoms Schematic depiction of the symptoms of dengue fever People infected with dengue virus are commonly asymptomatic or only have mild symptoms such as an uncomplicated fever.[1][2] Others have more severe illness, and in a small proportion it is life-threatening.[1] The incubation period (time between exposure and onset of symptoms) ranges from 3–14 days, but most often it is 4–7 days.[3] This means that travellers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home.[4] Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea),[5] but are more susceptible to the severe complications.[4] Clinical course The characteristic symptoms of dengue are: a sudden-onset fever, headache (typically behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "break-bone fever", comes from the associated muscle and joints pains.[1][6] The course of infection is divided into three phases: febrile, critical, and recovery.[7] The febrile phase involves high fevers, frequently over 40 °C (104 °F) and is associated with generalized pain and a headache; this usually lasts two to seven days.[6][7] Flushed skin and some small red spots called petechiae, which are caused by broken capillaries, may occur at this point,[7] as may some mild bleeding from mucous membranes of the mouth and nose.[4][6] The critical phase, if it occurs, follows the resolution of the high fever and typically lasts one to two days.[7] During this phase there may be significant fluid accumulation in the chest and abdominal cavity due to increased capillary permeability and leakage. This leads to depletion of fluid from the circulation and decreased blood supply to vital organs.[7] During this phase, organ dysfunction and severe bleeding (typically from the gastrointestinal tract) may occur.[4][7] Shock and hemorrhage occur in less than 5% of all cases of dengue,[4] however those who have previously been infected with other serotypes of dengue virus ("secondary infection") have an increased risk.[4][8] The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream.[7] This usually lasts two to three days.[4] The improvement is often striking, but there may be severe itching and a slow heart rate.[4][7] It is during this stage that a fluid overload state may occur, which if it affects the brain may reduce the level of consciousness or cause seizures.[4] Associated problems Dengue may occasionally affect several other body systems.[7] This may be either in isolation or along with the classic dengue symptoms.[5] A decreased level of consciousness occurs in 0.5–6% of severe cases. This may be caused by infection of the brain by the virus or indirectly due to impairment of vital organs, for example, the liver.[5][9] Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain-Barré syndrome.[5] Infection of the heart and acute liver failure are among the rarer complications of dengue.[4][7] Cause Virology Main article: Dengue virus A TEM micrograph showing dengue virus virions (the cluster of dark dots near the center) Dengue fever virus (DENV) is an RNA virus of the family Flaviviridae; genus Flavivirus. Other members of the same family include yellow fever virus, West Nile virus, St. Louis encephalitis virus, Japanese encephalitis virus, tick-borne encephalitis virus, Kyasanur forest disease virus, and Omsk hemorrhagic fever virus.[9] Most are transmitted by arthropods (mosquitoes or ticks), and are therefore also referred to as arboviruses (arthropod-borne viruses).[9] The dengue virus genome (genetic material) contains about 11,000 nucleotide bases, which code for the three different types of protein molecules that form the virus particle (C, prM and E) and seven other types of protein molecules (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) that are only found in infected host cells and are required for replication of the virus.[8][10] There are four strains of the virus, which are called serotypes, and these are referred to as DENV-1, DENV-2, DENV-3 and DENV-4.[2] All four serotypes can cause the full spectrum of disease.[8] Infection with one serotype is believed to produce lifelong immunity to that serotype but only short term protection against the others.[2][6] The severe complications on secondary infection seem to occur particularly if someone previously exposed to serotype DENV-1 then contracts serotype DENV-2 or serotype DENV-3, or if someone previously exposed to type DENV-3 then acquires DENV-2.[10] Transmission The mosquito Aedes aegypti feeding off a human host Dengue virus is primarily transmitted by Aedes mosquitoes, particularly A. aegypti.[2] These mosquitoes usually live between the latitudes of 35° North and 35° South below an elevation of 1,000 metres (3,300 ft).[2] They bite primarily during the day.[11] Other mosquito species—Aedes albopictus, A. polynesiensis and several A. scutellaris—may also transmit the disease.[2] Humans are the primary host of the virus,[2][9] but it may also circulate in nonhuman primates.[12] An infection may be acquired via a single bite.[13] A mosquito that takes a blood meal from a person infected with dengue fever becomes itself infected with the virus in the cells lining its gut. About 8–10 days later, the virus spreads to other tissues including the mosquito's salivary glands and is subsequently released into its saliva. The virus seems to have no detrimental effect on the mosquito, which remains infected for life. Aedes aegypti prefers to lay its eggs in artificial water containers and tends to live in close proximity to humans, and prefers to feed off people rather than other vertebrates.[14] Dengue may also be transmitted via infected blood products and through organ donation.[15][16] In countries such as Singapore, where dengue is endemic, the risk is estimated to be between 1.6 and 6 per 10,000 transfusions.[17] Vertical transmission (from mother to child) during pregnancy or at birth has been observed.[13] Other person-to-person modes of transmission have been reported, but are very unusual.[6] Predisposition Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished.[4] Women are more at risk than men.[10] Dengue may be life-threatening in people with chronic diseases such as diabetes and asthma.[10] It is thought that polymorphisms (normal variations) in particular genes may increase the risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin,[1] CTLA4, TGFβ,[8] DC-SIGN, and particular forms of human leukocyte antigen.[10] A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk.[18] Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection.[10] Mechanism When a mosquito carrying DENV bites a person, the virus enters the skin together with the mosquito's saliva. It binds to and enters white blood cells, and reproduces inside the cells while they move throughout the body. The white blood cells respond by producing a number of signalling proteins (such as interferon) that are responsible for many of the symptoms, such as the fever, the flu-like symptoms and the severe pains. In severe infection, the virus production inside the body is greatly increased, and many more organs (such as the liver and the bone marrow) can be affected, and fluid from the bloodstream leaks through the wall of small blood vessels into body cavities. As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs. Furthermore, dysfunction of the bone marrow leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue.[18] Viral reproduction After entering the skin, DENV binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens).[18] The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A.[8] DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main one.[10] The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is copied. Immature virus particles are transported to the Golgi apparatus, the part of the cell where the some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able enter other white blood cells (such as monocytes and macrophages).[8] The initial reaction of infected cells is to produce the interferon, a cytokine that raises a number of defenses against viral infection through the innate immune system by augmenting the production of a large group of proteins (mediated by the JAK-STAT pathway). Some serotypes of DENV appear to have mechanisms to slow down this process. Interferon also activates the adaptive immune system, which leads to the generation of antibodies against the virus as well as T cells that directly attack any cell infected with the virus.[8] Various antibodies are generated; some bind closely to the viral proteins and target them for phagocytosis (ingestion by specialized cells) and destruction, but some bind the virus less well and appear instead to deliver the virus into a part of the phagocytes where it is not destroyed but is able to replicate further.[8] Severe disease Further information: Antibody-dependent enhancement It is not entirely clear why secondary infection with a different strain of DENV places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction.[8][10] There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications,[1] and various lines of research have implied a role for T cells and soluble factors (such as cytokines and the complement system).[18] Severe disease is marked by two problems: dysfunction of endothelium (the cells that line blood vessels) and disordered blood clotting.[5] Endothelial dysfunction leads to the leakage of fluid from the blood vessels into the chest and abdominal cavities, while coagulation disorder is responsible for the bleeding complications. Higher levels of virus in the blood and involvement of other organs (such as the bone marrow and the liver) are associated with more severe disease. Cells in the affected organs die, leading to the release of cytokines and activation of both coagulation and fibrinolysis (the opposing systems of blood clotting and clot degradation). These alterations together lead to both endothelial dysfunction and coagulation disorder.[18] Diagnosis General Warning signs[19] Abdominal pain Ongoing vomiting Liver enlargement Mucosal bleeding High hematocrit with low platelets Lethargy The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas.[1] Early disease can however be difficult to differentiate from other viral infections.[4] A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area.[19] Warning signs typically occur before the onset of severe dengue.[7] The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely.[7] It may be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and occurs in similar parts of the world to dengue.[6] Often, investigations are performed to exclude other conditions that cause similar symptoms, such as malaria, leptospirosis, typhoid fever, and meningococcal disease.[4] The earliest change detectable on laboratory investigations is a low white blood cell count, which may then be followed by low platelets and metabolic acidosis.[4] In severe disease, plasma leakage may result in hemoconcentration (as indicated by a rising hematocrit) and hypoalbuminemia.[4] Pleural effusions or ascites may be detected by physical examination when large,[4] but the demonstration of fluid on ultrasound may assist in the early identification of dengue shock syndrome.[1][4] The use of ultrasound is limited by lack of availability in many settings.[1] Classification The World Health Organization's 2009 classification divides dengue fever into two groups: uncomplicated and severe.[1][19] This replaces the 1997 WHO classification, which needed to be simplified as it had been found to be too restrictive, but the older classification is still widely used.[19] The 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever.[4][20] Dengue hemorrhagic fever was subdivided further into four grades (grade I–IV). Grade I is the presence only of easy bruising or a positive "tourniquet test" (see below) in someone with fever, grade II is the presence of spontaneous bleeding into the skin and elsewhere, grade III is the clinical evidence of shock, and grade IV is shock so severe that blood pressure and pulse cannot be detected.[20] Grades III and IV are referred to as "dengue shock syndrome".[19][20] Virology and serology Dengue fever may also be diagnosed by microbiological laboratory testing.[19] This can be done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection or specific antibodies (serology).[10][21] Virus isolation and nucleic acid detection are more accurate than antigen detection, but these tests are not widely available due to their greater cost.[21] All tests may be negative in the early stages of the disease.[4][10] Apart from serology, laboratory tests are only of diagnostic value during the acute phase of the illness. Tests for dengue virus-specific antibodies, types IgG and IgM, can be useful in confirming a diagnosis in the later stages of the infection. Both IgG and IgM are produced after 5–7 days. The highest levels (titres) of IgM are detected following a primary infection, but IgM is also produced in secondary and tertiary infections. The IgM becomes undetectable 30–90 days after a primary infection, but earlier following re-infections. IgG, by contrast, remains detectable for over 60 years and, in the absence of symptoms, is a useful indicator of past infection. After a primary infection the IgG reaches peak levels in the blood after 14–21 days. In subsequent re-infections, levels peak earlier and the titres are usually higher. Both IgG and IgM provide protective immunity to the infecting serotype of the virus. In the laboratory test the IgG and the IgM antibodies can cross-react with other flaviviruses, such as yellow fever virus, which can make the interpretation of the serology difficult.[6][10][22] The detection of IgG alone is not considered diagnostic unless blood samples are collected 14 days apart and a greater than fourfold increase in levels of specific IgG is detected. In a person with symptoms, the detection of IgM is considered diagnostic.[22] Prevention A 1920s photograph of efforts to disperse standing water and thus decrease mosquito populations There are currently no approved vaccines for the dengue virus.[1] Prevention thus depends on control of and protection from the bites of the mosquito that transmits it.[11][23] The World Health Organization recommends an Integrated Vector Control program consisting of five elements: (1) Advocacy, social mobilization and legislation to ensure that public health bodies and communities are strengthened, (2) collaboration between the health and other sectors (public and private), (3) an integrated approach to disease control to maximize use of resources, (4) evidence-based decision making to ensure any interventions are targeted appropriately and (5) capacity-building to ensure an adequate response to the local situation.[11] The primary method of controlling A. aegypti is by eliminating its habitats.[11] This may be done by emptying containers of water or by adding insecticides or biological control agents to these areas.[11] Reducing open collections of water through environmental modification is the preferred method of control, given the concerns of negative health effect from insecticides and greater logistical difficulties with control agents.[11] People may prevent mosquito bites by wearing clothing that fully covers the skin and/or the application of insect repellent (DEET being the most effective).[13] Management There are no specific treatments for the dengue fever virus.[1] Treatment depends on the symptoms, varying from oral rehydration therapy at home with close follow-up, to hospital admission with administration of intravenous fluids and/or blood transfusion.[24] A decision for hospital admission is typically based on the presence of the "warning signs" listed in the table above, especially in those with preexisting health conditions.[4] Intravenous hydration is usually only needed for one or two days.[24] The rate of fluid administration is titrated to a urinary output of 0.5–1 mL/kg/hr, stable vital signs and normalization of hematocrit.[4] Invasive medical procedures such as nasogastric intubation, intramuscular injections and arterial punctures are avoided, in view of the bleeding risk.[4] Acetaminophen may be used for fever and discomfort while NSAIDs such as ibuprofen and aspirin are avoided as they might aggravate the risk of bleeding.[24] Blood transfusion is initiated early in patients presenting with unstable vital signs in the face of a decreasing hematocrit, rather than waiting for the hemoglobin concentration to decrease to some predetermined "transfusion trigger" level.[25] Packed red blood cells or whole blood are recommended, while platelets and fresh frozen plasma are usually not.[25] During the recovery phase intravenous fluids are discontinued to prevent a state of fluid overload.[4] If fluid overload occurs and vital signs are stable, stopping further fluid may be all that is needed.[25] If a person is outside of the critical phase, a loop diuretic such as furosemide may be used to eliminate excess fluid from the circulation.[25] Epidemiology See also: Dengue fever outbreaks Dengue distribution in 2006. Red: Epidemic dengue and Ae. aegypti Aqua: Just Ae. aegypti. Most people with dengue recover without any ongoing problems.[19] The mortality is 1–5% without treatment,[4] and less than 1% with adequate treatment.[19] Severe disease carries a mortality of 26%.[4] Dengue is believed to infect 50 to 100 million people worldwide a year with half a million life-threatening infections requiring hospitalization,[1] resulting in approximately 12,500–25,000 deaths.[5][26] The burden of disease from dengue is estimated to be similar to other childhood and tropical diseases, such as tuberculosis, at 1600 disability-adjusted life years per million population.[10] It is the most common viral disease transmitted by arthropods.[8] As a tropical disease it is deemed only second in importance to malaria.[4] It is endemic in more than 110 countries.[4] The World Health Organization counts dengue as one of sixteen neglected tropical diseases.[27] The incidence of dengue increased 30 fold between 1960 and 2010.[28] This increase is believed to be due to a combination of urbanization, population growth, increased international travel, and global warming.[1] The geographical distribution is around the equator with 70% of the total 2.5 billion people living in endemic areas from Asia and the Pacific.[28] In the United States, the rate of dengue infection among those who return from an endemic area with a fever is 2.9–8.0%,[13] and it is the second most common infection after malaria to be diagnosed in this group.[6] Until 2003, dengue was classified as a potential bioterrorism agent, but subsequent reports removed this classification as it was deemed too difficult to transfer and only caused hemorrhagic fever in a relatively small proportion of people.[29] History Etymology The origins of the word "dengue" are not clear, but one theory is that it is derived from the Swahili phrase Ka-dinga pepo, which describes the disease as being caused by an evil spirit.[30] The Swahili word dinga may possibly have its origin in the Spanish word dengue, meaning fastidious or careful, which would describe the gait of a person suffering the bone pain of dengue fever.[31] However, it is possible that the use of the Spanish word derived from the similar-sounding Swahili.[30] Slaves in the West Indies having contracted dengue were said to have the posture and gait of a dandy, and the disease was known as "dandy fever".[32][33] The term "break-bone fever" was first applied by physician and Founding Father Benjamin Rush, in a 1789 report of the 1780 epidemic in Philadelphia. In the report he uses primarily the more formal term "bilious remitting fever".[29][34] The term dengue fever came into general use only after 1828.[33] Other historical terms include "breakheart fever" and "la dengue".[33] Terms for severe disease include "infectious thrombocytopenic purpura" and "Philippine", "Thai", or "Singapore hemorrhagic fever".[33] Discovery The first record of a case of probable dengue fever is in a Chinese medical encyclopedia from the Jin Dynasty (265–420 AD) which referred to a "water poison" associated with flying insects.[30][35] There have been descriptions of epidemics in the 17th century, but the most plausible early reports of dengue epidemics are from 1779 and 1780, when an epidemic swept Asia, Africa and North America.[35] From that time until 1940, epidemics were infrequent.[35] In 1906, transmission by the Aedes mosquitoes was confirmed, and in 1907 dengue was the second disease (after yellow fever) that was shown to be caused by a virus.[36] Further investigations by John Burton Cleland and Joseph Franklin Siler completed the basic understanding of dengue transmission.[36] The marked rise of spread of dengue during and after the Second World War has been attributed to ecologic disruption. The same trends also led to the spread of different serotypes of the disease to different areas, and the emergence of dengue hemorrhagic fever, which was first reported in the Philippines in 1953. In the 1970s, it became a major cause of child mortality. Around the same time it emerged in the Pacific and the Americas.[35] Dengue hemorrhagic fever and dengue shock syndrome were first noted in Middle and Southern America in 1981, as DENV-2 was contracted by people who had previously been infected with DENV-1 several years earlier.[9] Research Current research efforts to prevent and treat dengue have included different means of vector control,[37] vaccine development, and antiviral drugs.[23] With regards to vector control, a number of novel methods have been used to reduce mosquito numbers with some success including the placement of the fish Poecilia reticulata or copepods in standing water to eat the mosquito larva.[37] There are ongoing programs working on a dengue vaccine to cover all four serotypes.[23] One of the concerns is that a vaccine may increase the risk of severe disease through antibody-dependent enhancement.[38] The ideal vaccine is safe, effective after one or two injections, covers all serotypes, does not contribute to ADE, is easily transported and stored, and is both affordable and cost-effective.[38] A number of vaccines are currently undergoing testing.[10][29][38] It is hoped that the first products will be commercially available by 2015.[23] Apart from attempts to control the spread of the Aedes mosquito and work to develop a vaccine against dengue, there are ongoing efforts to develop antiviral drugs that might be used to treat attacks of dengue fever and prevent severe complications.[39][40] Discovery of the structure of the viral proteins may aid the development of effective drugs.[40] There are several plausible targets. The first approach is inhibition of the viral RNA-dependent RNA polymerase (coded by NS5), which copies the viral genetic material, with nucleoside analogs. Secondly, it may be possible to develop specific inhibitors of the viral protease (coded by NS3), which splices viral proteins.[41] Finally, it may be possible to develop entry inhibitors, which stop the virus entering cells, or inhibitors of the 5' capping process, which is required for viral replication.[39] Notes ^ a b c d e f g h i j k l m Whitehorn J, Farrar J (2010). "Dengue". Br. Med. Bull. 95: 161–73. doi:10.1093/bmb/ldq019. PMID 20616106. ^ a b c d e f g WHO (2009), pp. 14–16 ^ Gubler (2010), p. 379 ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa Ranjit S, Kissoon N (July 2010). "Dengue hemorrhagic fever and shock syndromes". Pediatr. Crit. Care Med. 12 (1): 90–100. doi:10.1097/PCC.0b013e3181e911a7. PMID 20639791. ^ a b c d e f Varatharaj A (2010). "Encephalitis in the clinical spectrum of dengue infection". Neurol. India 58 (4): 585–91. doi:10.4103/0028-3886.68655. PMID 20739797. ^ a b c d e f g h Chen LH, Wilson ME (October 2010). "Dengue and chikungunya infections in travelers". Curr. Opin. Infect. Dis. 23 (5): 438–44. doi:10.1097/QCO.0b013e32833c1d16. PMID 20581669. ^ a b c d e f g h i j k l WHO (2009), pp. 25–27 ^ a b c d e f g h i j Rodenhuis-Zybert IA, Wilschut J, Smit JM (August 2010). "Dengue virus life cycle: viral and host factors modulating infectivity". Cell. Mol. Life Sci. 67 (16): 2773–86. doi:10.1007/s00018-010-0357-z. PMID 20372965. ^ a b c d e Gould EA, Solomon T (February 2008). "Pathogenic flaviviruses". The Lancet 371 (9611): 500–9. doi:10.1016/S0140-6736(08)60238-X. PMID 18262042. ^ a b c d e f g h i j k l m Guzman MG, Halstead SB, Artsob H, et al. (December 2010). "Dengue: a continuing global threat". Nat. Rev. Microbiol. 8 (12 Suppl): S7–S16. doi:10.1038/nrmicro2460. PMID 21079655. ^ a b c d e f WHO (2009), pp. 59–60 ^ "Vector-Borne Viral Infections". World Health Organization. Retrieved 17 January 2011. ^ a b c d Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book. Retrieved 2010-12-23. ^ Gubler (2010), pp. 377–78 ^ Wilder-Smith A, Chen LH, Massad E, Wilson ME (January 2009). "Threat of dengue to blood safety in dengue-endemic countries". Emerg. Infect. Dis. 15 (1): 8–11. doi:10.3201/eid1501.071097. PMC 2660677. PMID 19116042. ^ Stramer SL, Hollinger FB, Katz LM, et al. (August 2009). "Emerging infectious disease agents and their potential threat to transfusion safety". Transfusion 49 Suppl 2: 1S–29S. doi:10.1111/j.1537-2995.2009.02279.x. PMID 19686562. ^ Teo D, Ng LC, Lam S (April 2009). "Is dengue a threat to the blood supply?". Transfus Med 19 (2): 66–77. doi:10.1111/j.1365-3148.2009.00916.x. PMC 2713854. PMID 19392949. ^ a b c d e Martina BE, Koraka P, Osterhaus AD (October 2009). "Dengue virus pathogenesis: an integrated view". Clin. Microbiol. Rev. 22 (4): 564–81. doi:10.1128/CMR.00035-09. PMC 2772360. PMID 19822889. ^ a b c d e f g h WHO (2009), pp. 10–11 ^ a b c WHO (1997). "Chapter 2: clinical diagnosis". Dengue haemorrhagic fever: diagnosis, treatment, prevention and control (2nd ed.). Geneva: World Health Organization.. pp. 12–23. ISBN 9241545003. ^ a b WHO (2009), pp. 90–95 ^ a b Gubler (2010), p. 380 ^ a b c d WHO (2009), p. 137 ^ a b c WHO (2009), pp. 32–37 ^ a b c d WHO (2009), pp. 40–43 ^ WHO media centre (March 2009). "Dengue and dengue haemorrhagic fever". World Health Organization. Retrieved 2010-12-27. ^ Neglected Tropical Diseases. "Diseases covered by NTD Department". World Health Organization. Retrieved 2010-12-27. ^ a b WHO (2009), p. 3 ^ a b c Barrett AD, Stanberry LR (2009). Vaccines for biodefense and emerging and neglected diseases. San Diego: Academic. pp. 287–323. ISBN 0-12-369408-6. ^ a b c Anonymous (2006). "Etymologia: dengue". Emerg. Infec. Dis. 12 (6): 893. ^ Harper D (2001). "Etymology: dengue". Online Etymology Dictionary. Retrieved 2008-10-05. ^ Anonymous (1998-06-15). "Definition of Dandy fever". MedicineNet.com. Retrieved 2010-12-25. ^ a b c d Halstead SB (2008). Dengue (Tropical Medicine: Science and Practice). River Edge, N.J: Imperial College Press. pp. 1–10. ISBN 1-84816-228-6. ^ Rush AB (1789). "An account of the bilious remitting fever, as it appeared in Philadelphia in the summer and autumn of the year 1780". Medical enquiries and observations. Philadelphia, Pa.: Prichard and Hall. pp. 104–117. ^ a b c d Gubler DJ (July 1998). "Dengue and dengue hemorrhagic fever". Clin. Microbiol. Rev. 11 (3): 480–96. PMC 88892. PMID 9665979. ^ a b Henchal EA, Putnak JR (October 1990). "The dengue viruses". Clin. Microbiol. Rev. 3 (4): 376–96. PMC 358169. PMID 2224837. ^ a b WHO (2009), p. 71 ^ a b c Webster DP, Farrar J, Rowland-Jones S (November 2009). "Progress towards a dengue vaccine". Lancet Infect Dis 9 (11): 678–87. doi:10.1016/S1473-3099(09)70254-3. PMID 19850226. ^ a b Sampath A, Padmanabhan R (January 2009). "Molecular targets for flavivirus drug discovery". Antiviral Res. 81 (1): 6–15. doi:10.1016/j.antiviral.2008.08.004. PMC 2647018. PMID 18796313. ^ a b Noble CG, Chen YL, Dong H, et al. (March 2010). "Strategies for development of Dengue virus inhibitors". Antiviral Res. 85 (3): 450–62. doi:10.1016/j.antiviral.2009.12.011. PMID 20060421. ^ Tomlinson SM, Malmstrom RD, Watowich SJ (June 2009). "New approaches to structure-based discovery of dengue protease inhibitors". Infectious Disorders Drug Targets 9 (3): 327–43. PMID 19519486. References Gubler DJ (2010). "Dengue viruses". In Mahy BWJ, Van Regenmortel MHV. Desk Encyclopedia of Human and Medical Virology. Boston: Academic Press. ISBN 0-12-375147-0. WHO (2009). Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. World Health Organization. ISBN 9241547871. External links Find more about Dengue fever on Wikipedia's sister projects: Definitions from Wiktionary Images and media from Commons Learning resources from Wikiversity News stories from Wikinews Quotations from Wikiquote Source texts from Wikisource Textbooks from Wikibooks Dengue fever at the Open Directory Project "Dengue". WHO. Retrieved 2010-12-24. "Dengue". US Centers for Disease Control and Prevention. Retrieved 2010-12-24. "Dengue fever". UK Health Protection Agency. Retrieved 2010-12-24. [hide]v · d · eZoonotic viral diseases (A80–B34, 042–079) Arthropod/ (arbovirus) Mosquito Bunyaviridae Arbovirus encephalitis: La Crosse encephalitis (LCV) · California encephalitis (CEV) Viral hemorrhagic fever: Rift Valley fever (RVFV) Flaviviridae Arbovirus encephalitis: Japanese encephalitis (JEV) · Australian encephalitis (MVEV, KUNV) · St. Louis encephalitis (SLEV) · West Nile fever (WNV) Viral hemorrhagic fever: Dengue fever (DV) other: Yellow fever (YFV) · Zika fever Togaviridae Arbovirus encephalitis: Eastern equine encephalomyelitis (EEEV) · Western equine encephalomyelitis (WEEV) · Venezuelan equine encephalomyelitis (VEEV) other: Chikungunya (CV) · O'Nyong-nyong fever (OV) · Ross River fever (RRV) Tick Bunyaviridae Viral hemorrhagic fever: Crimean-Congo hemorrhagic fever (CCHFV) Flaviviridae Arbovirus encephalitis: Tick-borne encephalitis (TBEV) · Powassan encephalitis (PV) · Deer tick virus encephalitis (DTV) Viral hemorrhagic fever: Omsk hemorrhagic fever (OHFV) · Kyasanur forest disease (KFDV/Alkhurma virus)) · Langat virus (LGTV) Reoviridae Colorado tick fever (CTFV) Mammal Rodent (Robovirus) Arenaviridae Viral hemorrhagic fever: Lassa fever (LV) · Venezuelan hemorrhagic fever (Guanarito virus) · Argentine hemorrhagic fever (Junin virus) · Bolivian hemorrhagic fever (Machupo virus) · Lujo virus Bunyaviridae Puumala virus · Andes virus · Sin Nombre virus · Hantavirus (HV) Bat Filoviridae VHF: Ebola hemorrhagic fever · Marburg hemorrhagic fever Rhabdoviridae Australian bat lyssavirus · Mokola virus · Duvenhage virus · Lagos bat virus · Chandipura virus(sandfly) Bornaviridae Menangle · Henipavirus · Borna disease (Borna disease virus) Multiple Rhabdoviridae Rabies (RV) M: VIR virs(prot)/clss cutn/syst (hppv/hiva, infl/zost/zoon)/epon drugJ(dnaa, rnaa, rtva, vacc) Retrieved from "http://en.wikipedia.org/wiki/Dengue_fever"

Post a Comment