Dengue
fever (pronounced UK: /ˈdɛŋɡeɪ/, US: /ˈdɛŋɡiː/) and dengue
hemorrhagic fever (DHF) are acute febrile
diseases, found in the tropics, and caused by four closely related virus
serotypes of the genus Flavivirus, family Flaviviridae.[1] It is also known as breakbone fever. The geographical spread includes northern Australia, northern Argentina, and the entire Singapore, Malaysia, Taiwan,
Thailand, Cambodia, Vietnam, Indonesia, Honduras, Costa Rica, Panama,
Paraguay[2], Philippines, Pakistan, India, Sri Lanka, Bangladesh, Mexico,
Suriname, Dominican Republic, Puerto Rico, Jamaica, Bolivia[3], Brazil, Guyana,
Venezuela, Barbados, Trinidad and Samoa[4]. Unlike malaria, dengue is just as prevalent in the urban districts of
its range as in rural areas. 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 or more rarely the Aedes albopictus mosquito, which feed during the day.[5]
The WHO
says some 2.5 billion people, two fifths of the world's population, are now at
risk from dengue and estimates that there may be 50 million cases of dengue
infection worldwide every year. The disease is now epidemic in more than 100
countries.[6]
The disease manifests as a
sudden onset of severe headache, muscle and joint pains (myalgias and arthralgias—severe pain that gives it the
nick-name break-bone fever or bonecrusher disease), fever,
and rash.[7] The dengue rash is characteristically bright red petechiae and usually appears first on the lower limbs and the
chest; in some patients, it spreads to cover most of the body. There may also
be gastritis with some combination of associated abdominal pain, nausea, vomiting, or diarrhea. Some cases develop much milder
symptoms which can be misdiagnosed as influenza or other viral infection when no rash is present.
Thus travelers from tropical areas may pass on dengue in their home countries
inadvertently, having not been properly diagnosed at the height of their
illness. Patients with dengue can pass on the infection only through mosquitoes
or blood products and only while they are still febrile.
The classic dengue fever lasts about six to seven days, with a smaller peak of
fever at the trailing end of the disease (the so-called biphasic pattern).
Clinically, the platelet count will drop until the patient's temperature is
normal. Cases of DHF also show higher fever, variable haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion
of cases lead to dengue shock syndrome
(DSS) which has a high mortality rate. DHF combined with a cirrhotic liver has
been suspected in rapid development of hepatocellular carcinoma
(HCC). Given that the Dengue virus (DEN) is related to the Hepatitis C virus, this is an avenue for further research as
HCC is among the top five cancerous causes of death outside Europe
and North America. Normally HCC does not occur in a cirrhotic liver for ten or
more years after the cessation of the poisoning agent. DHF patients can develop
HCC within one year of cessation of poisoning agent.
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 - low platelet and white blood cell count. Care has to be taken as diagnosis of
DHF can mask end stage liver disease and vice versa.
- Fever, bladder problem, constant headaches, eye pain,
severe dizziness and loss of appetite.
- Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood,
or bloody diarrhea)
- Thrombocytopenia
(<100,000 platelets per mm³ or estimated as less than 3 platelets per
high power field)
- 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)
- Encephalitic occurrences.
A dependable immediate
information of the Dengue diagnostics in the rural areas can be performed by
the introduction of Rapid Diagnostic Test kits which also differentiates
between primary and secondary dengue infections. [8] Serology and polymerase chain reaction
(PCR) studies are available to confirm the diagnosis of dengue if clinically
indicated. Dengue can be a life threatening fever.
The mainstay of treatment
is timely supportive therapy to tackle shock due to hemoconcentration and
bleeding. Close monitoring of vital signs in critical period (between day 2 to
day 7 of fever) is critical. 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.[10]
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.[11] In vivo studies, however, have not yet been
done. Unlike HIV therapy, lack of adequate global interest and funding greatly
hampers the development of a treatment regime.
In Brazilian traditional medicine, dengue is treated with cat's claw herb, which is for inflammation and does not
prevent dengue.[12]
In Malaysia, dengue is treated by some using natural medicine. Mas Amirtha and Semalu developed by the
Alternative Medicine Research Institute, Center for Asia.[citation needed]
The treatment is speculated to be able to arrest and reverse the viral
infection and prevent the disease from advancing into a critical stage, though
no evidence has yet shown effectiveness. In Philippines dengue patients use
tawa-tawa herbs and sweet potato tops juice to increase the platelets counts
and revived the patients.[citation needed]
Dengue is transmitted by Aedes
mosquitoes, particularly A. aegypti and A. albopictus. Dengue may also be transmitted via infected
blood products (blood transfusions,
plasma, and platelets), but the scale of this problem is unknown.[13]
The first recognized Dengue
epidemics occurred almost simultaneously in Asia, Africa, and North America in
the 1780s, shortly after the identification and naming of the disease in 1779.
A pandemic began in Southeast Asia in the 1950s, and by 1975 DHF had become a
leading cause of death among children in the region. Epidemic dengue has become
more common since the 1980s. By the late 1990s, dengue was the most important
mosquito-borne disease affecting humans after malaria, with around 40 million
cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each
year. Significant outbreaks of dengue fever tend to occur every five or six months.
The cyclical rise and fall in numbers of dengue cases is thought to be the
result of seasonal cycles interacting with a short-lived cross-immunity[clarification needed]
for all four strains in people who have had dengue. When the cross-immunity
wears off the population is more susceptible to transmission whenever the next
seasonal peak occurs. Thus over time there remain large numbers of susceptible
people in affected populations despite previous outbreaks due to the four
different serotypes of dengue virus and the presence of unexposed
individuals from childbirth or immigration.
There is significant
evidence, originally suggested by S.B. Halstead in the 1970s, that dengue
hemorrhagic fever is more likely to occur in patients who have secondary
infections by another one of dengue fever's four serotypes. One model to
explain this process is known as antibody-dependent enhancement
(ADE), which allows for increased uptake and virion
replication during a secondary infection with a different strain. Through an
immunological phenomenon, known as original antigenic sin,
the immune system is not able to adequately respond to the
stronger infection, and the secondary infection becomes far more serious.[14] This process is also known as superinfection.[15][16]
There was a serious
outbreak in Rio de Janeiro in February
2002 affecting around one million people and killing sixteen. On March 20,
2008, the secretary of health of the state of Rio de Janeiro,
Sérgio Côrtes, announced that 23,555 cases of dengue, including 30 deaths, had
been recorded in the state in less than three months. Côrtes said, "I am
treating this as an epidemic because the number of cases is extremely
high." Federal Minister of Health, José Gomes Temporão also announced that
he was forming a panel to respond to the situation. Cesar Maia, mayor of the city of Rio de Janeiro, denied that there was serious cause for
concern, saying that the incidence of cases was in fact declining from a peak
at the beginning of February. [17] By April 3, 2008, the number of cases reported rose
to 55,000 [18]
In Singapore, there are 4,000–5,000 reported cases of dengue
fever or dengue haemorrhagic fever every year. In the year 2004, there were
seven deaths from dengue shock syndrome[19].
An outbreak of dengue fever
was declared in Cairns, located in the tropical north of Queensland, Australia on 1 December 2008. As at 3
March 2009 there were 503 confirmed cases of dengue fever, in a residential
population of 152,137. Outbreaks were subsequently declared the neighbouring
cities and towns of Townsville (outbreak declared 5 January
2009), Port Douglas (6 February 2009), Yarrabah (19 February 2009), Injinoo (24
February 2009), Innisfail (27 February 2009) and Rockhampton (10 March 2009). There have been occurrences of
dengue types one, two, three and four in the region. March 4 2009, Queensland
Health had confirmed an elderly woman had died from dengue fever in Cairns, in
the first fatality since the epidemic began last year. The statement said that
although the woman had other health problems, she tested positive for dengue
and the disease probably contributed to her death.
In 2009, in Argentina, a dengue outbreak was declared the northern
provinces of Chaco, Catamarca, Salta, Jujuy, and Corrientes, with over 9673
cases reported as of April 11, 2009 by the Health Ministry [1]. Some travelers from the affected zones have spread the
fever as far south as Buenos Aires [2]. Major efforts to control the epidemic in Argentina are focused on preventing its vector (the Aedes
mosquitoes) from reproducing. This is addressed by asking people to dry out all
possible water reservoirs from where mosquitoes could proliferate (which is, in
other countries, known as "descacharrado"). There have also been
information campaigns concerning prevention of the dengue fever; and the
government is fumigating with insecticide in order to control the mosquito
population.[20]
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.[22] 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.[23] A number of other vaccine candidates are entering phase I or II testing.[24]
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.
Primary prevention of
dengue mainly resides in mosquito control. There
are two primary methods: larval control and adult mosquito control.[citation needed]
In urban areas, Aedes mosquitos breed on water collections in artificial
containers such as plastic cups, used tires, broken bottles, flower pots, etc.
Periodic draining or removal of artificial containers is the most effective way
of reducing the breeding grounds for mosquitos.[citation needed]
Larvicide treatment is another effective way to control the
vector larvae but the larvicide chosen should be long-lasting and preferably
have World Health Organization clearance for use in drinking water. There are
some very effective insect growth regulators
(IGRs) available which are both safe and long-lasting (e.g. pyriproxyfen). For reducing the adult mosquito load, fogging
with insecticide is somewhat effective.[citation needed]
Prevention of mosquito
bites is another way of preventing disease. This can be achieved by using insect repellent, mosquito traps or mosquito nets.
In 1998, scientists from
the Queensland
Institute of Medical Research (QIMR) 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.[25] This method is viewed as being more cost-effective
and more environmentally friendly than pesticides, though not as effective, and
requires the continuing participation of the community.[26]
Even though this method of
mosquito control was successful in rural provinces, not much is known about how
effective it could be if applied to cities and urban areas. The Mesocyclops can survive and breed in large water
containers, but would not be able to do so in small containers of which most
urban area have within their homes. Also, Mesocyclops are hosts for the guinea worm, a pathogen that
causes a parasite infection, and so this method of mosquito control cannot be
used in countries that are still susceptible to the guinea worm. The biggest dilemma with Mesocyclops is that its success depends on the
participation of the community. This idea of a possible parasite bearing
creature in household water containers dissuades people from continuing the
process of inoculation, and without the support and work of everyone living in
the city, this method would not be successful.[27]
In 2004, scientists from
the Federal University of Minas
Gerais, Brazil, discovered a fast way to find and count mosquito
population inside urban areas. The technology, named Intelligent Monitoring of
Dengue (in Portuguese), uses traps with kairomones that capture Aedes
gravid females, and upload insect counts with a combination of cell phone, GPS
and internet technology. The result is a complete map of the
mosquitoes in urban areas, updated in real time and accessible remotely, that
can inform control methodologies.[28] The technology was recognized with a Tech Museum Award in 2006.[29]
In 2009, scientists from
the School of Integrative Biology at The University of Queensland
revealed that by infecting Aedes mosquitos with the bacterium Wolbachia, the
adult lifespan was reduced by half. [30] In the study, super-fine needles were used to
inject 10,000 mosquito embryos with the bacterium. Once an insect was infected,
the bacterium would spread via its eggs to the next generation. A pilot release
of infected mosquitoes could begin in Vietnam within three years. If no
problems are discovered, a full-scale biological attack against the insects
could be launched within five years. [31]
Dengue
virus belongs to the family Flaviviridae, which includes the hepatitis C virus, West Nile and Yellow fever viruses among others. Possible laboratory-based
modification of the yellow fever vaccine YF-17D to target the dengue virus via chimeric replacement has been discussed extensively in
scientific literature.[32] To date, however, no full scale studies have been conducted.[33]
In 2006, a group of
Argentine scientists discovered the molecular replication mechanism of the
virus, which could be specifically attacked by disrupting the viral RNA polymerase.[34] In cell culture[35] and murine experiments,[36][37] morpholino antisense oligos have shown
specific activity against Dengue virus.
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.[39] 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.[40] Alternatively, the use of the Spanish word may
derive from the similar-sounding Swahili.[41]
Also known as "Dandy
Fever", slaves in the West Indies who contracted dengue were said to have
the posture and gait of a dandy. [42]
The first recorded
potential case of dengue fever comes from a Chinese medical encyclopedia from
the Jin Dynasty (265–420 AD). The Chinese referred to a “water
poison” associated with flying insects. [41] The first definitive case report dates from 1789
and is attributed to Benjamin Rush, who coined the term
"breakbone fever" because of the symptoms of myalgia and arthralgia.[43] The viral etiology and the transmission by mosquitoes were deciphered
only in the 20th century. Population movements during World War II spread the
disease globally. A pandemic of dengue began in Southeast Asia
after World War II and has spread around the globe since then.[44]
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