Mosquito Sting: A Host of Parasites and Virions
Dhrubo Jyoti Sen,
Jimit S. Patel, Charoo S. Garg, Divyang H. Shah, Kiran M. Patel, Dhara S. Bhavsar, Tirtha V. Patel, Dhara M. Limbachia
Department of Pharmaceutical
Chemistry, Shri Sarvajanik
Pharmacy College, Gujarat Technological University, Arvind
Baug, Mehsana-384001, Gujarat, India,
ABSTRACT:
Mosquitoes are a vector agent that carries mosquito-borne
disease, transmitting viruses and parasites from person to person without catching the disease
themselves. Mosquitoes carrying these viruses stay healthy while carrying them
because their immune system recognizes them as bad and "chops
off" the virus's genetic coding, rendering it harmless. It is currently
unknown how they handle parasites so they can safely carry them. Infection of
humans occurs when a mosquito bites someone while its immune system is still in
the process of destroying the virus's harmful coding. Female mosquitoes suck
blood from people and other animals as part of their eating and breeding
habits. Mosquito borne diseases are prevalent in more than 100 countries,
infecting 300-500 million people and causing about 1 million deaths every year.
In India, more than 40 million people suffer from mosquito diseases annually.
There are a number of diseases borne by mosquitoes. They are malaria, filaria, dengue, brain fever and yellow fever. Yellow fever
is caused by mosquitoes in jungle areas in parts of Africa and South America.
In India, malaria, filaria and dengue are the most
prevalent diseases spread by mosquitoes. The diseases continue to explode from
time to time. The reason is that these mosquitoes develop resistance to
medicines and chemicals. Hence fighting mosquitoes and the diseases spread by
them is a continuous process.
KEYWORDS: virus genetic code,
malaria, encephalitis, filarial, dengue, brain fever, yellow fever, drug
resistance.
INTRODUCTION:
In the past, mosquito-borne disease presented a severe
problem for early western to all the zone of the world. That
mosquito-transmitted blood parasite sustained to be a trouble in many parts of
the U.S. into the early 1950's, when it was brought under control by
eliminating the human source of infection. Humans infected with the parasite
are the only cause of malaria contamination, and with the appearance of efficient
medicine, window screens and an improved understanding of mosquitoes and the
infection, human malaria in the U. S. was eliminated. Malaria is not the lone
mosquito-borne disease that has caused troubles in the earlier period, even
into the early 1940's hundreds of cases of equine encephalitis were accounted
in the mid-west and west every year. It wasn't until the 1950's nevertheless
that the first human cases of mosquito-borne encephalitis were acknowledged.
Even nowadays human and equine cases of encephalitis are not unusual happenings.For example, in Colorado in 1987, 45 horse and
30 human cases of Western Equine Encephalitis (WEE) were diagnosed. Also, in
the same year 6 human cases of St. Louis Encephalitis (SLE) were accounted. In
1991, 1 human and 1 horse case of WEE was reported in the very same state. In
2002 everything changed, West Nile Virus arrived in Colorado.1
Mosquito life cycle:
The mosquito goes through four separate and distinct
stages of its life cycle and they are as follows: Egg, Larva, pupa, and adult.
Each of these stages can be easily recognized by their special appearance.
There are four common groups of mosquitoes living in the Bay Area. They are Aedes, Anopheles, Culex,
and Culiseta.
Egg: Eggs are laid one at a time and they float on the
surface of the water. In the case of Culex
and Culiseta species,
the eggs are stuck together in rafts of a hundred or more eggs. Anopheles
and Aedes species do not make egg
rafts but lay their eggs separately. Culex,
Culiseta, and Anopheles lay their
eggs on water while Aedes lay
their eggs on damp soil that will be flooded by water. Most eggs hatch into
larvae within 48 hours.
Larva: The larva (larvae - plural) lives in the water and
come to the surface to breathe. They shed their skin four times growing larger
after each molting. Most larvae have siphon tubes for breathing and hang from
the water surface. Anopheles larvae do not have a siphon and they
lay parallel to the water surface.
The larva feed on micro-organisms and organic matter in
the water. On the fourth molt the larva changes into a pupa.
Pupa: The pupal stage is a
resting, non-feeding stage. This is the time the mosquito turns into an adult.
It takes about two days before the adult is fully developed. When development
is complete, the pupal skin splits and the mosquito
emerges as an adult.
Adult: The newly emerged adult rests on the surface of the
water for a short time to allow itself to dry and all its parts to harden.
Also, the wings have to spread out and dry properly before it can fly. The egg,
larvae and pupae stages depend on temperature and species characteristics as to
how long it takes for development. For instance, Culex
tarsalis might go through its life cycle in 14
days at 70 F and take only 10 days at 80 F. Also, some species have naturally
adapted to go through their entire life cycle in as little as four days or as
long as one month.2
Figure-1: Picture of Female
mosquito Anopheles
Figure-2: General life-cycle
of Mosquito
INTRODUCTION:
There seem to be more mosquito borne diseases and
epidemic fears sweeping the nation than there ever were before. This is
understandable - especially when there is a possibility that the small bug
sucking on your arm could be transferring one of these diseases:
·
Malaria
·
Yellow Fever
·
Dengue Fever
·
West Nile Virus
·
Arboviral Encephilitides
That is not to say that every
bite will be lethal. Most mosquito
bites are nothing but annoying.
However, in a time when there are so many diseases, it is best to protect
yourself the best you can to ensure that you don't become the next victim of a
mosquito borne illness. This article discusses the four main mosquito-borne
diseases that can be transmitted to humans, and reviews each diseases symptom.
That is the malaria, yellow fever,
dengue fever, west Nile virus and somewhat Encephalitis. Mosquitoes can
cause more than itchy, annoying bumps. These flying insects have the potential to infect humans with
several different potentially dangerous and deadly diseases. In the United
States, mosquito-related deaths are rare, but they can and do occur. Those who
are planning to travel abroad, should be aware of the types of mosquito
transmitted diseases, preventative measures one can take, as well as the
symptoms and urgency of treatment should infection occur. Here we will discuss about the four main mosquito-borne diseases.3
Malaria is quite rare in the United States,
but affects 300 to 500 million people worldwide, and can have dangerous and
even deadly consequences. This parasitic disease can be transmitted from
infected mosquitoes to humans.
There are three stages of malaria infection.
The cold
stage can cause symptoms such as
fever, shaking and chills.
The hot
stage can cause symptoms such as
nausea and vomiting, high fever, dizziness, delirium, headache and pain.
The sweating
stage can cause symptoms such as
splenomegaly, decreased body temperature, hepatomegaly, sweating, fever and chills, fatigue,
shortness of breath, anemia, pale skin and extreme exhaustion. Those who
suspect that they have malaria need to get medical attention immediately so
that they can begin treatment and have the best chance of avoiding serious
health complications and death.4
LIFE CYCLE OF MALARIA:
Female Anopheles mosquito carrying
malaria-causing parasites feeds in a human and injects the parasites in the
form of sporozoites into the bloodstream. The sporozoites travel to the liver and invade liver cells.
Over 5-16 days, the sporozoites
grow, divide, and produce tens of thousands of haploid forms, called merozoites, per liver cell. Some malaria parasite species
remain dormant for extended periods in the liver, causing relapses weeks or
months later.
The merozoites exit
the liver cells and re-enter the bloodstream, beginning a cycle of invasion of
red blood cells, asexual replication, and release of newly formed merozoites from the red blood cells repeatedly over 1-3
days. This multiplication can result in thousands of parasite-infected cells in
the host bloodstream, leading to illness and complications of malaria that can
last for months if not treated.
Some of the merozoites
-infected blood cells leave the cycle of asexual multiplication. Instead of
replicating, the merozoites in these cells develop
into sexual forms of the parasite, called male and female gametocytes that
circulate in the bloodstream.
Figure-3: Life
cycle of malaria parasite
When a mosquito bites an infected human, it ingests
the gametocytes. In the mosquito gut, the infected human blood cells burst,
releasing the gametocytes, which develop further into mature sex cells called
gametes. Male and female gametes fuse to form diploid zygotes, which develop
into actively moving ookinetes that burrow into the
mosquito midgut wall and form oocysts.
Growth and division of each oocyst
produces thousands of active haploid forms called sporozoites.
After 8-15 days, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from
which they travel to and invade the mosquito salivary glands. The cycle of
human infection re-starts when the mosquito takes a blood meal, injecting the sporozoites from its salivary glands into the human
bloodstream.
The mosquitoes that transmit malaria are found in some
areas, not any of the major cities. These mosquitoes generally bite around
sunset and sunrise. Malaria transmitting mosquitoes are usually found near the
Cambodian border (especially near the seaside) and the Burma border.5
Symptoms of malaria:
sudden high fever and chills, muscle aches and headaches. They usually show up
after an incubation time of 7 to 30 days. To be properly diagnosed with
malaria, you must undergo a blood smear examination, which all major hospitals
and many clinics can administer. There are drug-resistant strains of malaria,
and it's important to tell the doctor where you've been because the particular
drug resistance varies by region.6
The early symptoms of this disease
typically last two to five days and can include headache, nausea and vomiting,
muscle pain, high fever, kidney inflammation, furry tongue, irritability,
slowed pulse, decreased urine, bloodshot eyes, constipation, facial flushing
and proteinurea.
Those with yellow fever will often
experience a remission lasting a few hours or a few days. Once the remission is
over the yellow phase begins and lasts for about three to nine days.
The symptoms associated with the yellow
phase can include most of the early symptoms plus; jaundice, convulsions, bleeding,
confusion, hemorrhage, renal damage, bruising, weakness, acute fever, slowed
heartbeat, diarrhea, bloody vomit or black vomit, hematuria,
liver inflammation, chest and abdominal pain and yellow skin. Coma and death
can also occur. Those who suspect that they have this disease need to seek
medical attention immediately to begin treatment and to try and avoid serious
medical complications, coma and death.8
Transmission of the yellow fever virus in the animals:
·
Sylvatic (jungle) cycle: In tropical rainforests, yellow fever virus
is endemic among lower primates. Infected monkeys pass the virus to mosquitoes
that feed on them. Persons who subsequently enter the forest (often workers, eg, loggers, and travelers) are infected with this form of
disease. In Africa, the principal vector of the jungle cycle is Aedes africanus; in
South America, Haemogogus janthinomys is the primary vector for jungle
transmission. Nonhuman primates remain the preferred host in this setting.
Figure-4: Transmission of yellow fever virus
·
Intermediate
(savannah) cycle: In moist and semihumid areas of
Africa, semi-domestic mosquitoes (that breed in the wild and around households)
will feed primarily on monkeys but also on humans when the opportunity arises.
This cycle likely reflects the evolution of yellow fever into an epidemic human
disease. It is the most common cycle present in Africa and frequently leads to
small-scale outbreaks within villages. It can potentially develop into
large-scale epidemics if an infected individual carries the disease into an
urban region. This cycle has not been identified in South America.
·
Urban cycle: Aedes aegypti is
responsible for the transmission of urban yellow fever in both Africa and South
America. This mosquito has the ability to transmit the virus from person to
person and infect large populations of unvaccinated individuals. Urban
outbreaks are rare in South America, yet they are still occasionally reported
in densely populated regions in Africa.9
The disease "dengue fever" is carried by a
particular species of mosquito, the Aedes aegypti mosquito, which is active all day. It is on the
rise to becoming one of the top public health problems in the tropics.
The mosquito which carries this virus is most common in
urban areas around human dwellings, and is most active during the daytime. The Aedes mosquito breeds in clear water.
Dengue fever is an acute viral disease and an
infectious disease that can be transmitted from mosquitoes to humans. Epidemics
of dengue are growing, and it is currently estimated that 50 to 100 million
people develop this disease each year throughout more than
100 countries.10
Symptoms
usually start to appear between 5 and 7 days after being bitten. The symptoms
include severe headaches, high fever which may fluctuate, bone aches (hence the
slang name), joint and muscle pains, nausea and vomiting, and a rash of small
red spots a few days after the onset of fever. Dengue fever is a very serious
illness abd require immediately for treatment. It can
become fatal if the symptoms are allowed to progress over time to DHF (Dengue
Hemorrhagic Fever), which is characterized by heavy bleeding, though DHF is
thought to affect mainly longterm residents who have
picked up more than one strain of the virus. Aspirin should be avoided, because
aspirin reduces blood clotting and thus makes hemorrage
more likely. There is no vaccine against dengue fever, and no specific
treatment. You'll have to follow the doctor's orders. Dengue fever is often
mistaken for malaria, the flu (influenza) or something else. Malaria can be
excluded by a blood test, and the indication of dengue can be inferred by a
blood test. Recovery will take time, with tiredness sometimes lasting several
weeks. Research revealed that the Aedes aegypti mosquito
that carries dengue does not travel far from its breeding place, unlike other
species of mosquito, which explains why dengue outbreaks tend to occur in
localized areas of a few hundred meters radius. It is believed that dengue
spread by infected human migrant workers more than migrant mosquitoes.
Therefore, when an outbreak can be determined in a particular location, the
authorities may come and spray. However, given that urban dwellers tend to
travel around the city and symptoms start around 5 to 7 days later, it's not
always clear where the infection occured.11
There are several clinical forms of dengue
fever:
-
Asymptomatic dengue
fever: the patience does not feel ill.
-
Classical
dengue : high fever with debilitating fatigue ; intense muscle aches
and pain, occasionally unbearable
headaches, the appearance of itchy red patches on the body. The illness lasts
from 4 to 8 days but convalescence may take longer.
-
Dengue haemorrhagic fever: the same as above but with persistent
fever and external and internal haemorrhagic symptoms
(bleeding).
-
Dengue shock syndrome:
the same as above but with the onset of a state of shock.
The latter two forms, more frequent in
children, can be fatal if left untreated. Any of the four serotypes can cause
any of the various clinical forms. A diagnosis of dengue fever can only be
given with certainty after lab tests (risk of confusion with influenza, leptospirosis, malaria, etc.) that either directly look for
the virus or proceed by detecting antibodies to it. While it is possible
to alleviate the symptoms of dengue, there is no known remedy to fight the
virus itself. In addition, no safe and effective vaccine is available
currently. The only way to control this disease is to reduce the vector
mosquito population as much as possible. Such control is all the more necessary
since more and more regions of the world are being affected by dengue fever and
the haemorrhagic form seems to be appearing with
increasing frequency.12
Transmission of Dengue fever:
Mosquitoes usually
pick up the Dengue virus while feeding on
the blood of an infected person, the virus incubates for a
period of up to 10 days and an infected mosquito is capable, during probing and
blood feeding, of transmitting the virus for
the rest of its life. It is also suspected that infected female mosquitoes may
transmit the virus to their offspring by transovarial (via the eggs) transmission, but how relevant
this in sustaining transmission of the virus
to humans remains unclear.13
So while infected
mosquitoes are the culprits in spreading the disease it is infected humans who
are the main carriers and multipliers of the virus, as they provide a source for uninfected
mosquitoes. The virus circulates in the blood
of infected humans for two to seven days and this is when symptoms appear and
the Aedes mosquitoes may acquire the virus when they feed on an individual during this period - some
research has shown that monkeys in some parts of the world also play a similar
role in the transmission of the dengue virus.
1. When drinking the blood of a viraemic human (virus present in the peripheral blood), the
female mosquito takes in a certain number of viral particles.
2. The viruses move up with the ingested blood
into the oesophagus.
3. They end up in the stomach where they resist
the mosquitos digestive juices.
4. Given the high degree of adaptation between the
virus and its vector, the viral particles are able to break through the stomach
wall barrier and after a latency phase, they multiply with great intensity
inside the mosquitos cells.
5. While invading all parts of the mosquitos
body, the virus enters the salivary glands where it concentrates.
6. The next time the female A.aegypti
bites a healthy person to take a blood meal; it injects saliva that acts as
an anaesthetic,
a lubricant for the mobile mouth parts, an anticoagulant and an aid to
digestion due to the enzymes it contains.
7.While doing this, it also injects a certain amount of virus
which, if the person is not immune, will bring on the disease.
Figure-5:
Transmission of dengue virus
(Phase 1) and Phase 6) are separated by a period of
about 10 to 14 days called the extrinsic incubation period. The length of time
does, however, depend on the temperature. After that, the female remains
infectious for the rest of its life. This diagram applies to almost all
the arboviruses transmitted by mosquitoes. In some
cases, vertical tranmission may occur, which means
that an infected female can transmit the virus to its eggs and therefore
to its offspring.14
The term West Nile mosquito or
mosquito West Nile Virus does not mean that one must travel to the other side
of the world to come into contact with this insect. Year by year, it seems like
more and more West Nile mosquito bite cases are popping up all over the United
States. Now viewed as a seasonal epidemic in North America, summer and fall
seem to be the times when it shines. West Nile virus is the most common
mosquito-borne illness in the United States. The Center for Disease Control
(CDC) tracks the activity and spread of this illness and has worked to raise
awareness of simple protective measures one can take, such as the elimination
of common breeding grounds for mosquitos and the
application of mosquito repellent. First making an appearance in North America
in 1999, coming with reports of infected humans and horses, it claimed 18 lives
in its first year. Reports show that there were 3,598 humans infected with the
mosquito West Nile Virus by the year 2007. While not everyone who is infected
by a diseased mosquito's bite will meet death, at least 200 of those people are
expected to develop some type of serious illness. Everyone should protect
themselves from the possibility of the West Nile Virus. A constant awareness of
one's surroundings should assist in that protection. This is even truer for
children and for those over 50. The older or younger one is, the more
susceptible they are to this growing deadly disease. The symptoms
of West Nile virus can include fever, seizures, neck pain, lethargy, headache,
coma, body aches, malaise, rash, fatigue, muscle aches, stiff neck, swollen
lymph nodes, diarrhea, weakness, photophobia, nausea and vomiting, altered
mental state and maculopapular rash. This is a very
serious disease that needs to be treated by a doctor immediately for the best
outcome.15
Transmission of West Nile virus:
The first step in the
transmission cycle of West Nile virus (WNV) happens when a mosquito bites an
infected bird or animal and gets the virus while feeding on the animal's blood.
The infected mosquito can then transmit the virus to another bird or animal
when it feeds again.
Crows are highly susceptible to
lethal infection, as are robins, blue jays, and other birds. Scientists have
identified more than 138 bird species that can be infected and more than 43
mosquito species that can transmit WNV. Although the virus usually cycles
between mosquitoes and birds, infected female mosquitoes also can transmit WNV
through their bites to humans and other "incidental hosts," such as
horses. With so many susceptible hosts to amplify the virus and so many types
of mosquitoes to transmit it, WNV has spread rapidly across the United States.
Most cases of human disease occur in elderly people and in people with impaired
immune systems. WNV also can be transmitted through blood transfusions and
organ transplants from WNV-infected donors. Health experts also believe it is
possible for WNV to be transmitted from a mother to her unborn child and
through breast milk.16
Figure-6:
Transmission of Wet Nile virus
Encephalitis:
Encephalitis in various forms such as St. Louis,
Western Equine, La Crosse, Eastern Equine, and West Nile, which was recently
discovered in the Northeast, is endemic to the United States and increasing in
incidence. Although extremely rare, Eastern Equine Encephalitis has a 30% - 60%
mortality rate once contracted. Severe damage to the central nervous system
occurs in those that survive the illness. Eastern Equine Encephalitis (EEE) is
maintained in nature through a cycle between the Culiseta
melanura mosquito and birds that live in freshwater
swamps. Although Culiseta melanura
do not bite humans, some mosquitoes will "cross bite"; i.e., bite an
infected bird and then bite a human or animal (horse, emu, and other exotic
birds), thereby spreading the disease. These mosquitoes are also known as
"bridge vectors". A vector is a species that transmits a disease from
one host to another. These bridge vectors may take a meal from a bird and later
take another meal from a mammal. Symptoms usually occur within two to ten days
after being bitten by an infected mosquito. These symptoms include high fever,
stiff neck, headache, confusion, and lethargy. Encephalitis, swelling of the
brain, is the most dangerous symptom. Rhode Island has confirmed five cases of
EEE with two deaths in the last thirteen years. The last death was reported in
1993.
Encephalitis is an acute
inflammation
of the brain.
Encephalitis with meningitis is known as meningoencephalitis.
Symptoms include headache, fever, confusion, drowsiness, and fatigue. More advanced and serious symptoms include seizures
or convulsions,
tremors,
hallucinations,
and memory problems.17
Viral encephalitis can be
due either to the direct effects of an acute infection, or as one of the sequelae of a latent infection. A common cause of
encephalitis in humans is herpes simplex virus type I (HSE) which may cause
inflammation of the brain. This can result in death. Others include infection
by Flaviviruses such as St. Louis encephalitis or
West Nile virus, or Togaviruses such as Eastern
equine encephalitis (EEE), Western equine encephalitis (WEE) and Venezuelen equine encephalitis (VEE).
It can be caused by a bacterial
infection, such as bacterial meningitis, spreading directly to the brain (primary
encephalitis), or may be a complication of a current infectious disease syphilis
(secondary encephalitis). Certain parasitic
or protozoal infestations, such as toxoplasmosis,
malaria,
or primary amoebic meningoencephalitis,
can also cause encephalitis in people with compromised
immune
systems. Lyme disease and/or Bartonella
henselae may also cause encephalitis. Another cause
is granulomatous amoebic encephalitis.18
Adult patients with
encephalitis present with acute onset of fever, headache, confusion, and
sometimes seizures. Younger children or infants may present irritability, poor
appetite and fever. Neurological examinations usually reveal a drowsy or
confused patient. Stiff neck, due to the irritation of the meninges
covering the brain, indicates that the patient has either meningitis or meningoncephalitis. Examination of the cerebrospinal fluid obtained by a lumbar
puncture procedure usually reveals increased amounts of protein and
white blood cells with normal glucose, though in a significant percentage of
patients, the cerebrospinal fluid may be normal. CT scan often is not helpful, as cerebral
abscess is uncommon. Cerebral abscess is more common in patients with
meningitis than encephalitis. Bleeding is also uncommon except in patients with
herpes
simplex type 1 encephalitis. Magnetic resonance imaging offers better
resolution. In patients with herpes simplex encephalitis, electroencephalograph
may show sharp waves in one or both of the temporal lobes. Lumbar puncture
procedure is performed only after the possibility of prominent brain swelling
is excluded by a CT scan examination. Diagnosis is often made with detection of
antibodies in the cerebrospinal fluid against a specific viral agent (such as
herpes simplex virus) or by polymerase chain reaction that amplifies
the RNA
or DNA of the
virus responsible (such as varicella zoster virus).19
Treatment is usually symptomatic.
Reliably tested specific antiviral agents are available only for a few viral
agents (e.g. acyclovir
for herpes simplex virus) and are used with
limited success for most infection except herpes simplex encephalitis. In
patients who are very sick, supportive treatment, such as mechanical
ventilation, is equally important. Corticosteroids (e.g. methylprednisolone)
are used to reduce brain swelling and inflammation. Sedatives may be needed for
irritability or restlessness.20
Encephalitis lethargica is an atypical form of
encephalitis which caused an epidemic from 1918 to 1930. Those who survived sank into a
semi-conscious state that lasted for decades until the Parkinson's drug L-DOPA was used
to revive those still alive in the late 1960s by Oliver Sacks.
There have been only a
small number of isolated cases in the years since, though in recent years a few
patients have shown very similar symptoms. The cause is now thought to be
either a bacterial agent or an autoimmune response following infection.21
In a
large number of cases, called limbic encephalitis, the pathogens responsible
for encephalitis attack primarily the limbic system
(a collection of structures at the base of the brain responsible for emotions
and many other basic functions).
Arboviral Encephilitiedes:
While the term Arboviral Encephilitiedes may
sound ridiculous, any time you hear the phrase Arboviral
Encephilitides mosquito borne illness you should be concerned.
Encephilitides are viral diseases transferred by
mosquitoes that can cause inflammation of the brain. In extreme cases, this
inflammation eventually can lead the infected person to experience brain
damage, fall into a coma, or even meet death.22
Brain damage and death is the
total extreme when it comes to these diseases. Most infected persons end up
with less minor flu-like symptoms which include:
·
Headaches
·
Muscle Aches
·
Fever
·
Malaise
For most, symptoms never even
surface. For some, the symptoms are much more extreme than flu-like.
·
High Fever
·
Confusion
·
Stiff Back
·
Stiff Neck
·
Sensitivity to
Light
·
Vomiting
There are a few varieties of Encephalitides found in the United States. These varieties
include:
·
Eastern Equine
Encephalitis
·
Western Equine
Encephalitis
·
St. Louis
Encephalitis
·
La Crosse
Encephalitis (LAC)
·
West Nile
Encephalitis
Out of all these varieties of
mosquito illnesses, the Eastern Equine is viewed as the most deadly. Even with
only an average of four deaths a year in the United States, it is one of the
mosquito illnesses that could someday affect a much larger portion of the
population.23-26
Minimizing Mosquito Bites:
There various ways to minimize mosquito bites:
·
Apply
anti-mosquito lotions and sprays. Tests by consumer magazines show that many
popular ones do not actually last long. The best are icaridin and DEET. DEET is most commonly sold despite criticisms of
toxicity, but it does not significantly affect the vast majority of people. (It
does not kill or actually repel mosquitoes, either; it just stops mosquitoes
from recognizing you as prey by blocking their senses.) Apply it to clothes and
unbroken skin, but avoid ingestion and don't use it on infants. Mosquitoes are
immensely worse than DEET. The next best alternatives seem to be eucalyptus
(eucalyptol) and citronella oil.
·
Cover your body
with clothes, including thick socks, even if you wear sandals
·
It's said that mosquitoes
are more attracted to dark colors, so wear white, maybe even thin nightwear
·
Do not apply
perfumes and colognes
·
At restaurants,
request mosquito coils and places them upwind.
·
At home, cover any
standing water (such as the urns), deal with any places that hold rainwater,
and for any ponds with lotus flowers and the like you should add some small
fish that eat mosquito larvae
·
Get a mosquito net
for travelling with
·
Notably, tests
show that electronic mosquito killers and repellers
do not kill a significant fraction of the mosquito population.
N,N-Diethyl-meta-toluamide Permethrin
Allathrine Icaridin
Structures of the Mosquito Repellents:
The best ways to kill mosquitoes in your home are with
your hands, insecticide spray, or electronic rackets sold at superstores.
Insecticide spray can have side effects such as headaches, especially for
children. Most mosquitoes are most active around sunrise and sunset, which is
why you see a peak in activity around these times, but some mosquitoes are
active all times of the day and night. Some species seek shelter during the
heat of the day. Mosquitoes eat flower nectar and some other things. Only
female mosquitoes bite humans, as they need the protein to make their eggs.27-30
CONCLUSION:
At the last, mosquitoes are one of the prime vect0r
agents which spreads the number of diseases to death
through viruses and parasites by withdrawing immune system of a person, so
prevention must be taken and full treatment must be provided until complete
recovery has been achieved.
ACKNOWLEDGEMENT:
All the authors are thankful to the search engine of
library of SSPC, Mehsana for data collection of
various aspects of mosquito borne diseases.
REFERENCES:
1.
Fradin, M. S. "Mosquitoes and mosquito repellents: a
clinician's guide". Annals of
Internal Medicine 128 (11): 931940, 1998.
2.
Dale RC, Church AJ, Surtees RA, et
al. "Encephalitis
lethargica syndrome: 20 new cases and evidence of
basal ganglia autoimmunity". Brain 127: 2133, 2004.
3.
Stryker Sue B. "Encephalitis lethargica: the behavior residuals". Training
School Bulletin 22: 1527, 1925.
4.
Reid AH, McCall S, Henry JM, Taubenberger JK. "Experimenting on the past: the
enigma of von Economo's encephalitis lethargica". J. Neuropathol.
Exp. Neurol. 60 (7): 66370,
2001.
5.
Vilensky JA,
Goetz CG, Gilman S. "Movement disorders associated with encephalitis lethargica: a video compilation". Mov.
Disord. 21 (1): 18, 2006.
6.
McCall S, Vilensky
JA, Gilman S, Taubenberger JK. "The
relationship between encephalitis lethargica and
influenza: a critical analysis". J. Neurovirol.
14 (3): 17785, 2008.
7.
Vilensky JA,
Foley P, Gilman S. "Children
and encephalitis lethargica: a historical
review". Pediatr. Neurol.
37 (2): 7984, 2007.
8.
Haeman,
Jang; David Boltz, Katharine Sturm-Ramirez, Kennie R. Shepherd, Yun Jiao,
Robert Webster, Richard J. Smeyne. "Highly
pathogenic H5N1 influenza virus can enter the central nervous system and induce
neuroinflammation and neurodegeneration".
Proceedings of the National Academy of Sciences 106 (33): 14063, 2009.
9.
Blunt SB, Lane RJ, Turjanski N, Perkin GD. "Clinical features and
management of two cases of encephalitis lethargica".
Mov. Disord. 12 (3): 3549, 1997.
10. Olejnik E. "Infectious
adenitis transmitted by Culex molestus". Bull Res Counc
Isr 2:
2101, 1952.
11. Smithburn KC, Jacobs HR.
"Neutralization-tests against neurotropic
viruses with sera collected in central Africa". Journal of Immunology
44: 923, 1942.
12.
Tsai TF, Popovici
F, Cernescu C, Campbell GL, Nedelcu
NI. "West
Nile encephalitis epidemic in southeastern Romania". Lancet
352 (9130): 76771, 1998.
13. Sejvar JJ, Haddad MB, Tierney
BC, et al. "Neurologic manifestations and outcome of West Nile virus
infection". JAMA 290 (4): 5115, 2003.
14.
Ahmed S, Libman
R, Wesson K, Ahmed F, Einberg K. "Guillain-Barrι syndrome: An unusual presentation of West
Nile virus infection". Neurology 55 (1): 1446, 2000.
15.
Abroug F, Ouanes-Besbes L, Letaief M, et
al. "A cluster study of predictors of severe West Nile virus
infection". Mayo Clin. Proc. 81 (1): 126, 2006.
16.
Perelman A, Stern J. "Acute
pancreatitis in West Nile Fever". Am. J. Trop. Med. Hyg. 23
(6): 11502, 1974.
17. Omalu BI, Shakir
AA, Wang G, Lipkin WI, Wiley CA. "Fatal fulminant pan-meningo-polioencephalitis due to West Nile virus". Brain Pathol. 13
(4): 46572, 2003.
18.
Mathiot CC,
Georges AJ, Deubel V. "Comparative analysis of
West Nile virus strains isolated from human and animal hosts using monoclonal
antibodies and cDNA restriction digest
profiles". Res. Virol. 141 (5): 53343, 1990.
19.
Hayes EB, Komar
N, Nasci RS, Montgomery SP, O'Leary DR, Campbell GL. "Epidemiology
and transmission dynamics of West Nile virus disease". Emerging
Infect. Dis. 11 (8):
116773, 2005.
20.
Fonseca DM, et al. (March
2004). "Emerging vectors in the Culex pipiens complex". Science 303 (5663): 15358, 2004.
21.
Spielman A, et
al. "Outbreak of West Nile Virus in North America". Science
306 (5701): 14735, 2004.
22. Centers
for Disease Control and Prevention. "Laboratory-acquired West Nile virus
infectionsUnited States, 2002". MMWR Morb.
Mortal. Wkly. Rep. 51 (50):
11335, 2002.
23.
Fonseca K, Prince GD, Bratvold J, et al. "West Nile virus infection
and conjunctival exposure". Emerging Infect.
Dis. 11 (10): 16489, 2005.
24.
Centers for Disease Control and
Prevention. "Investigation of blood transfusion recipients with West Nile
virus infections". MMWR Morb. Mortal. Wkly.
Rep. 51 (36): 823, 2002.
25.
Panthier R, Hannoun C, Beytout D, Mouchet J. "[Epidemiology of West Nile virus. Study of
a center in Camargue.]" (in
French). Ann Inst Pasteur (Paris) 115 (3): 43545, 1968.
26.
Kumar D, Drebot
MA, Wong SJ, et al. "A seroprevalence
study of west nile virus infection in solid organ
transplant recipients". Am. J. Transplant. 4 (11): 18838, 2004.
27.
Glass, WG; Lim JK, Cholera R, Pletnev AG, Gao JL, Murphy PM. "Chemokine receptor CCR5 promotes leukocyte trafficking to
the brain and survival in West Nile virus infection". Journal
of Experimental Medicine 202
(8): 108798, 2005.
28.
Glass, WG; McDermott DH, Lim JK, Lekhong S, Yu SF, Frank WA, Pape
J, Cheshier RC, Murphy PM. "CCR5 deficiency
increases risk of symptomatic West Nile virus infection". Journal
of Experimental Medicine 203
(1): 3540, 2006.
29.
Schneider BS, Soong L, Zeidner NS, Higgs S. "Aedes aegypti salivary gland extracts modulate anti-viral and
TH1/TH2 cytokine responses to sindbis virus
infection". Viral Immunol. 17 (4): 56573, 2004.
30.
Hayes EB, Gubler
DJ. "West Nile virus: epidemiology and clinical features of an emerging
epidemic in the United States". Annu.
Rev. Med. 57: 18194, 2006.
Received on 10.03.2011
Modified on 23.03.2011
Accepted
on 11.04.2011
©
A&V Publication all right reserved
Research
J. Science and Tech. 3(3): May-June.
2011: 119-126