E ASTERN M EDITERRANEAN A RBOVIRUSES Sogol Sheikh-Akbari

EASTERN MEDITERRANEAN ARBOVIRUSES

Sogol Sheikh-Akbari

INTRODUCTION (1)

The word arbovirus is an ecological term used to describe viruses that require a blood-sucking arthropod to complete their life cycle. By definition, arboviruses require a minimum of two hosts, a vertebrate and an arthropod.

Arboviruses are taxonomically diverse, belonging to 8 viral families and 14 genera. Most arboviruses of public health importance belong to 3 families: Flaviviridae, Togaviridae, and Bunyaviridae.

INTRODUCTION (2)

The arboviruses are, zoonoses that depend on animal species other than humans for maintenance in nature. Humans generally are dead-end or incidental hosts who usually do not contribute to the transmission cycle by developing viremia and infecting arthropods.

The most important arboviruses are those that cause major masquito-borne epidemics because they produce viremia in humans.

INTRODUCTION (3)

The most important reservoir hosts for arboviruses are birds or rodents, and the most important arthropod vectors are mosquitoes and ticks.

Arboviruses as a group have a global distribution, but the majority are found in tropical areas where climate conditions permit year-round transmission by cold-blooded arthropods.

INTRODUCTION (4)

Individual arboviruses may have a focal geographic distribution that is limited by the ecological parameters governing their transmission cycle. In general, the important limiting factors include temperature, rainfall patterns, and humidity, which in turn influence vegetation patterns and other ecological parameters that determine the geographic distribution of arthropod vectors and vertebrate hosts.

THE EASTERN MEDITERRANEN COUNTRIES

EMR : Bahrain, Cyprus, Islamic Republic of Iran,

Jordan, Kuwait, Lebanon, Libyan Arab Jamahiriya, Oman, Qatar, Saudi Arabia, Syrian Arab Republic, Tunisia, United Arab Emirates, Afghanistan, Djibouti, Egypt, Iraq, Morocco, Pakistan, Somalia, Sudan, Yemen.

THE WORLD DISTRIBUTION OF ARBOVIRUSES

DENGUE/DENGUE HEMORRHAGIC FEVER (1)

DF/DHF are caused by the dengue viruses, which belong to the genus Flavivirus, family Flaviviridae. There are four antigenically related, but distinct, dengue virus serotypes (DEN-1, DEN-2, DEN-3 and DEN-4). The four serotypes of dengue virus are phylogenetically distinct, and often to the same degree as different "species" of flaviviruses.


Description: Dengue virus is transmitted in a cycle involving humans and mosquitoes, Aedes aegypti being the most important vector.

Two distinct transmission cycles have been described for DENV: Endemic and epidemic cycles that occur in urban/periurban environments and involve human reservoir and amplification hosts.


The peridomestic mosquito Ae. aegypti is the principal DENV vector, with Ae. albopictus and other anthropophilic Aedes mosquitoes serving as secondary vectors.


Replication and Transmission of Dengue virus:

1. Virus transmitted to human in mosquito salvia

2. Virus replicates in target organs3. Virus infects white blood cells and lymphatic

tissues4. Virus released and circulates in blood5. Second mosquito ingests virus with blood6. Virus replicates in mosquito midgut and other

organs, infects salivary glands7. Virus replicates in salivary glands



Dengue Clinical Syndromes:

Undifferentiated fever Classic Dengue fever ( fever, headache,

muscle and joint pain, nausea and vomiting, rash, hemorrhagic manifestations)

Dengue hemorrhagic fever Dengue shock syndrome


Unusual Presentations of Severe Dengue Fever:

Encephalopathy Hepatic damage Cardiomyopathy Severe gastrointestinal hemorrhage

DENGUE/DENGUE HEMORRHAGIC FEVER)8)

Hypothesis on Pathogenesis of DHF:

Persons who have experienced a Dengue infection develop serum Abs that can neutralize the Dengue virus of that same (homologous) serotype.

In a subsequent infection, the pre-existing heterologous Abs form complexes with the new infecting virus serotype, but do not neutralize the new virus.

DENGUE/DENGUE HEMORRHAGIC FEVER)9)

Antibody-dependent enhancement is the process in which certain strains of Dengue virus, complexed with non-neutralizing Abs, can enter a greater proportion of cells of the mononuclear lineage, thus increasing virus production.

Infected monocytes release vasoactive mediators, resulting in increased vascular permeability and hemorrhagic manifestations that characterize DHF and DSS.

DENGUE/DENGUE HEMORRHAGIC FEVER(10)

Treatment:

There is no specific medication for treatment of a Dengue infection. The person should use pain relievers with acetaminophen and avoid those containing aspirin. They should also rest and drink plenty of fluids.


Where do the outbreaks of Dengue occur?

Outbreaks of dengue occur primarily in areas where Aedes aegypti (sometimes also Aedes albopictus) mosquitoes live. This includes most tropical urban areas of the world. Dengue viruses may be introduced into areas by travelers who become infected while visiting other areas of the tropics where dengue commonly exists.



One to four Dengue viruses may be endemic in the same human population; generally they are associated with only mild illness (silent transmission) during inter-epidemic periods but cause epidemics associated with more severe disease every 3-5 years.

Co-circulation of various virus serotypes in a community (hyperendemicity) is the single most common risk factor associated with the emergence of the severe form of disease –DHF- in an area.


Other important factors are: a combination of the increased movement of

viruses in people among countries and regions, the level of herd immunity to specific virus serotypes in human population, and genetic changes in circulating or introduced viruses that given them greater epidemic potential


Increased disease incidence and epidemic activity are closely correlated with trends of increased population growth in urban areas of the tropical developing world, increased movement of people among population centers via modern transportation, and lack of effective mosquito control.

The disease is endemic in the Americas, southeast Asia, western Pacific, Africa and the eastern Mediterranean, with the major disease burden in the three first regions.


CRIMEAN-CONGO HEMORRHAGIC FEVER(1)

Crimean-Congo haemorrhagic fever (CCHF) is a viral haemorrhagic fever of the Nairovirus group. Although primarily a zoonosis, sporadic cases and outbreaks of CCHF affecting humans do occur. The disease is endemic in many countries in Africa, Europe and Asia, and during 2001, cases or outbreaks have been recorded in Kosovo, Albania, Iran, Pakistan, and South Africa.


The disease was first described in the Crimea in 1944 and given the name Crimean hemorrhagic fever. In 1969 it was recognized that the pathogen causing Crimean hemorrhagic fever was the same as that responsible for an illness identified in 1956 in the Congo, and linkage of the 2 place names resulted in the current name for the disease and the virus. CCHF is a severe disease in humans, with a high mortality rate. Fortunately, human illness occurs infrequently, although animal infection may be more common.


The geographical distribution of the virus, like that of its tick vector, is widespread. Evidence of CCHF virus has been found in Africa, Asia, the Middle East and Eastern Europe.




CCHF Virus: The virus which causes CCHF is a Nairovirus,

a group of related viruses forming one of the five genera in the Bunyaviridae family of viruses.

Spread and Transmission: Ixodid ticks, especially those of the genus,

Hyalomma, are both a reservoir and a vector for the CCHF virus.


Numerous wild and domestic animals, such as cattle, goats, and sheep , serve as amplifying hosts for the virus.

Transmission to humans occurs through contact with infected animal blood or ticks. CCHF can be transmitted from one infected human to another by contact with infectious blood or body fluids.



Symptoms:

The onset of CCHF is sudden, with initial signs and symptoms including headache, high fever, back pain, joint pain, stomach pain, and vomiting. Symptoms may also include jaundice, and in severe cases, changes in mood.


Treatment: General supportive therapy is the mainstay

of patient management in CCHF. Intensive monitoring to guide volume and blood component replacement is required.

The antiviral drug ribavirin has been used in treatment of established CCHF infection with apparent benefit. Both oral and intravenous formulations seem to be effective.


Prevention and Control: Although an inactivated, mouse brain-

derived vaccine against CCHF has been developed and used on a small scale in Eastern Europe, there is no safe and effective vaccine widely available for human use. The tick vectors are numerous and widespread and tick control with acaricides (chemicals intended to kill ticks) is only a realistic option for well-managed livestock production facilities.


Persons living in endemic areas should use personal protective measures that include avoidance of areas where tick vectors are abundant and when they are active (Spring to Fall); regular examination of clothing and skin for ticks, and their removal; and use of repellents.

YELLOW FEVER(1)

Yellow fever is a viral disease that has caused large epidemics in Africa and the Americas. Infection causes a wide spectrum of disease, from mild symptoms to severe illness and death. The "yellow" in the name is explained by the jaundice that affects some patients. Although an effective vaccine has been available for 60 years, the number of people infected over the last two decades has increased and yellow fever is now a serious public health issue again.

YELLOW FEVER(2)

Cause:

The disease is caused by the yellow fever virus, which belongs to the flavivirus group. In Africa there are two distinct genetic types (called topotypes) associated with East and West Africa. South America has two different types, but since 1974 only one has been identified as the cause of disease outbreaks.

YELLOW FEVER(3)

Symptoms: Two disease phases: While some infections

have no symptoms whatsoever, the first, "acute", phase is normally characterized by fever, muscle pain , headache, shivers, loss of appetite, nausea and/or vomiting. The high fever is paradoxically associated with a slow pulse. After three to four days most patients improve and their symptoms disappear.

YELLOW FEVER(4)

15% enter a "toxic phase" within 24 hours. Fever reappears. The patient rapidly develops jaundice and complains of abdominal pain with vomiting. Bleeding can occur from the mouth, nose, eyes and/or stomach. Blood appears in the vomit and faeces. Kidney function deteriorates; this can range from abnormal protein levels in the urine to complete kidney failure with no urine production (anuria). Half of the patients in the "toxic phase" die within 10-14 days. The remainder recover without significant organ damage.

YELLOW FEVER(5)

Transmission: Humans and monkeys are the principal

animals to be infected. The virus is carried from one animal to another (horizontal transmission) by a biting mosquito (the vector). The mosquito can also pass the virus via infected eggs to its offspring (vertical transmission). The eggs produced are resistant to drying and lie dormant through dry conditions, hatching when the rainy season begins. Therefore, the mosquito is the true reservoir of the virus, ensuring transmission from one year to the next.

YELLOW FEVER(6)

Several different species of the Aedes and Haemogogus mosquitoes transmit the yellow fever virus. Any region populated with these mosquitoes can potentially harbour the disease.

Regions affected: The virus is constantly present with low

levels of infection (i.e. endemic) in some tropical areas of Africa and the Americas. This viral presence can amplify into regular epidemics.

YELLOW FEVER(7)

Thirty-three countries, with a combined population of 508 million, are at risk in Africa. Although yellow fever has never been reported from Asia, this region is at risk because the appropriate primates and mosquitoes are present.

YELLOW FEVER(8)

YELLOW FEVER(9)

YELLOW FEVER(10)

Infection of Humans: There are 3 cycles for yellow fever and they all exist

in Africa.1. Sylvatic (or jungle) yellow fever: In tropical

rainforests, yellow fever occurs in monkeys that are infected by wild mosquitoes. The infected

monkeys can then pass the virus onto other mosquitoes that feed on them. These infected wild mosquitoes bite humans entering the forest resulting in sporadic cases of yellow fever.

2. Intermediate yellow fever: In humid or semi-humid savannahs of Africa, small-scale epidemics occur.

YELLOW FEVER(11)

These behave differently from urban epidemics; many separate villages in an area suffer cases simultaneously, but fewer people die from infection. Semi-domestic mosquitoes infect both monkey and human hosts. This area is often called the "zone of emergence", where increased contact between man and infected mosquito leads to disease. This is the most common type of outbreak seen in recent decades in Africa. It can shift to a more severe urban-type epidemic if the infection is carried into a suitable environment (with the presence of domestic mosquitoes and unvaccinated humans).

YELLOW FEVER (12)

3. Urban yellow fever: Large epidemics can occur when migrants introduce the virus into areas with high human population density. Domestic mosquitoes (of one species, Aedes aegypti) carry the virus from person to person; no monkeys are involved in transmission. These outbreaks tend to spread outwards from one source to cover a wide area.

YELLOW FEVER (13)

Treatment and Prevention:

There is no specific treatment for yellow fever. Any superimposed bacterial infection should be treated with an appropriate antibiotic.

YELLOW FEVER (14)

Yellow fever vaccine is safe and highly effective. The protective effect (immunity) occurs within one week in 95% of people vaccinated. A single dose of vaccine provides protection for 10 years and probably for life.

A major concern at the beginning of the 21st century is that urban YF epidemics will once again occur in the American tropics.

YELLOW FEVER(15)

If this occurs in today’s world of modern transportation and crowded urban populations, and with increasingly rapid movement of larger numbers of people among population centers, YF, like DEN viruses, will spread rapidly throughout the American region, and from there most likely to Asian and Pacific countries, most of which are heavily infested with Ae. Aegypti.

YELLOW FEVER(16) YF has never been documented in Asia.

There are 3 possible reasons for this:1. Past urban YF epidemics occurred in the

Americas and West Africa before modern transportation, and the simple logistics of introducing YF virus into Asia were much more difficult than at present. While YF virus was probably introduced, it was most likely a rare occurrence, and the probability of a person incubating YF virus and arriving in an area in which there were adequate Ae. Aegypti mosquitoes to initiate secondary transmission was very low.

YELLOW FEVER(17)

2. Ae. aegypti mosquitoes in Asia may not be as susceptible to YF virus as those in the Americas and Africa.

3. A number of other flaviviruses are endemic to Asia, mainly the four dengue serotypes and JE, and most residents of Asian countries have detectable flavivirus antibodies.

RIFT VALLEY FEVER(1)

Rift Valley Fever (RVF) is a viral zoonosis that primarily affects animals but also has the capacity to infect humans. Infection can cause severe disease in both animals and humans, leading to high rates of disease and death.

RVF virus is a member of the Phlebovirus genus, one of the five genera in the family Bunyaviridae. The virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley of Kenya. Since then, outbreaks have been reported in sub-Saharan and North Africa.


In 1997-98, a major outbreak occurred in Kenya, Somalia and Tanzania and in September 2000, RVF cases were confirmed in Saudi Arabia and Yemen, marking the first reported occurrence of the disease outside the African continent and raising concerns that it could extend to other parts of Asia and Europe.


Transmission to Humans:

direct or indirect contact with the blood or organs of infected animals

Ingesting the unpasteurized or uncooked milk of infected animals

Bites of infected mosquitoes (most commonly Aedes)

To date, no human-to-human transmission of RVF has been documented.


Symptoms of RVF:

People with RVF typically have either no symptoms or a mild illness associated with fever and liver abnormalities.

In some patients the illness can progress to hemorrhagic fever, encephalitis , or ocular disease.


Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and extreme weight loss at the onset of the illness. Typically, patients recover within two days to one week after onset of illness.

Approximately 1% of humans that become infected with RVF die of the disease.


Complications After Recovery:

The most common complication associated with RVF is inflammation of the retina. As a result, approximately 1% - 10% of affected patients may have some permanent vision loss.

Acute hepatitis is another complication which may be seen in some cases.


Treatment and Vaccine:

There is no treatment, but ribavirin, interferon, immune modulators, and convalescent-phase plasma may help the patient.

An inactivated vaccine has been developed for human use. However, this vaccine is not licensed and is not commercially available.

RIFT VALLEY FEVER( (8

Prevention:

Decreasing contact with mosquitoes and other bloodsucking insects through the use of mosquito repellents and bednets.

Avoiding exposure to blood or tissues of animals that may potentially be infected


Epidemiology:

Epizootics of RVF are unique because they often do not begin in one place and spread to other areas. Rather, they erupt almost simultaneously over wide geographic areas in association with increased rainfall.

Although epizootics/epidemics of RVF have occurred over the majority of sub-Saharan Africa, the virus has expanded its geographic distribution in the past 25 years.


Epidemics occurred in Egypt in 1977, in Somalia and Kenya in 1998, and then the virus entered Saudi Arabia and Yemen in 2000.

How was the virus introduced into Egypt or Middle East?

It may have been transported in infected domestic animals.

It may have been introduced by infected Aedes mosquitoes flying from Africa.


The potential for future movement of this virus is great because the virus infects a wide variety of domestic animals, and causes a high level of viremia in many, has a very broad mosquito host range, and is capable of transovarial transmission.



WEST NILE VIRUS(1)

West Nile virus was discovered in 1937 in the West Nile district of Uganda. It is a member of the Japanese encephalitis serogroup of the genus flavivirus and the family Flaviviridae.

West Nile virus is transmitted to humans by the bite of an infected mosquito. Mosquitoes become infected by biting birds that harbor the virus. The virus is not spread from person to person or from infected birds to humans without a mosquito bite. The virus has now been found in 111 bird species and about a dozen mammals.

WEST NILE VIRUS(2)

WNV is established as a seasonal epidemic in that flares up in the summer and continues into the fall.

How does West Nile Virus spread? Infected mosquitoes (Culex) Transfusions, transplants, and mother-to-

child

WEST NILE VIRUS(3)

Symptoms:1. Serious symptoms in a few people (high

fever, headache, coma, muscle weakness, vision loss, numbness and paralysis ). The virus can cause encephalitis and meningitis.

2. Milder symptoms in some people (fever, headache, and body aches, nausea, vomiting, and sometimes swollen lymph glands or a skin rash on the chest, stomach and back)

3. No symptoms in most people

WEST NILE VIRUS(4)

Treatment: There is no known effective antiviral

treatment or vaccine to prevent West Nile virus.

In severe cases of West Nile virus, intensive supportive therapy is indicated. This includes hospitalization, IV fluids and nutrition, airway management, prevention of secondary infections, as well as good nursing care.

WEST NILE VIRUS (5)

Epidemiology: West Nile virus was first isolated from a

person with a nonspecific febrile illness in Uganda in 1937. It was not observed again until the 1950s, when WN virus was shown to be widespread in the Middle East and India and caused outbreaks of human disease in Israel.

Other than sporadic epidemics in France (1962) and South Africa (1974 and 1983–1984) and occasional isolations from vertebrate hosts or mosquitoes, WN virus was rarely seen and was considered of only minor importance to public health.

WEST NILE VIRUS(6) In the mid-1990s, the epidemiology of WN

virus apparently changed. Epizootics and epidemics of severe neurologic disease in horses, birds, and humans began to occur with increasing frequency.

The reasons for this dramatic emergence of epizootic/epidemic disease caused by a virus that rarely gave rise to severe disease are not well understood, but a new more virulent strain of virus with greater epidemic potential likely emerged and was propagated in the Mediterranean region and subsequently spread to new geographic regions in the late 1990s.

WEST NILE VIRUS(7)

There have been outbreaks of WN virus in Morocco in 1996, and in Tunisia in 1997.

WN virus moves north in spring and south in fall with migrating birds.

Prevention and control of epidemic/epizootic disease must rely on active surveillance and effective mosquito control.

WEST NILE VIRUS(8)

SANDFLY FEVER(1)

Sandfly fever which is also called three day fever, papatasi fever and phlebotomous fever is one of the arbovirus diseases which can be transmitted via bite and transovarial transmission of virus within phlebotomous species.

The important serotypes are Sicilian, Naples, Toscana, Karimabad and Salehabad.

SANDFLY FEVER(2)

Sand fly fever is a viral infection; symptoms include headache, fever, conjunctival infection (red eyes), tiredness, nausea and pain in the limbs, back and eyes. The symptoms are self-limiting and can last up to one week.

The virus circulates among rodents, domestic animals and human, and P. papatasi is the main vector.

SANDFLY FEVER(3)

This viral disease is transmitted by the bite of an infected sand fly. These flies usually bite at night and are small enough to get through the holes in a standard mosquito net.

The dominant serotype in Iran is karim-abad.

SANDFLY FEVER(4)

SANDFLY FEVER(5)

Prevention:

Use an effective repellent. Bed nets should be impregnated with an insecticide to prevent the tiny flies getting though the mesh. In very high risk areas, travellers may consider treating their clothes with insecticides. There is no vaccine.

SANDFLY FEVER(6)

Treatment:

There is no specific treatment for sand fly fever. Medications can be used to manage symptoms of pain.

KYASANUR FOREST DISEASE(1)

Kyasanur forest disease (KFD) is caused by Kyasanur forest disease virus (KFDV), a member of the virus family Flaviviridae. KFDV was identified in 1957 when it was isolated from a sick monkey from the Kyasanur forest in the Karnataka State, India.

KFD is limited to Karnataka State, India. Recently, however, a virus very similar to KFD virus was discovered in Saudi Arabia.


How does KFDV spread to humans?

The main hosts of KFDV are small rodents, but bats, and monkeys may also carry the virus. KFD is transmitted from the bite of an infected tick (Haemaphysalis spinigera is the major vector). Humans can get these diseases from a tick bite or by contact with an infected animal, such as sick or recently dead monkey.


Larger animals such as goats, cows, and sheep may become infected with KFD, but they do not have a role in the transmission of the disease.

There is no evidence of the disease being transmitted via the unpasteurized milk of any of these animals.


Symptoms:

The symptoms begin suddenly with fever, headache, severe muscle pain, cough, dehydration, gastrointestinal symptoms and bleeding problems.

Patients may experience abnormally low blood pressure, and low platelet, red blood cell, and white blood cell counts.


After 1-2 weeks of symptoms, some patients recover without complication. However, in most patients, the illness is biphasic and the patient begins experiencing a second wave of symptoms at the beginning of the third week. These symptoms include fever and signs of encephalitis.

There are approximately 400-500 cases of KFD per year with a case fatality rate of 3% to 5%.


Treatment: There is no specific treatment for KFD, but

supportive therapy is important.

Prevention: There is no vaccine available for KFD.

Utilizing insect repellents and wearing protective clothing in areas where ticks are endemic is recommended.

JAPANESE ENCEPHALITIS (1)

JE virus (JEV) is a member of the genus Flavivirus in the family Flaviviridae, together with YFV and DV.

All these viruses are transmitted by Culex mosquitoes. Wild birds and pigs play a major role in the enzootic cycle of JEV, which replicates in both species and in the mosquito. Humans occasionally may be bitten by an infected mosquito but are dead-end hosts and contribute little to the spread of the natural infection.


Symptoms:

Most JE infections are asymptomatic. Clinical disease varies from a nonspecific febrile illness, which may include cough, nausea, vomiting, diarrhea and photophobia, to a severe disease with meningoencephalitis, aseptic meningitis or a polio-like paralysis.


JE is a leading cause of severe central nervous system infection in Asia and Australia, where 30,000–50,000 cases are reported annually. About 30–35% are fatal. Large outbreaks of JE, often involving adults, have been reported on the Indian subcontinent, and the disease is currently considered hyperendemic in northern India and southern Nepal as well as in parts of central and southern India. The spread of JE in new areas has been correlated with agricultural development and intensive rice cultivation supported by irrigation programmes.




There is no specific therapy. Intensive supportive therapy is indicated.

Purified formalin-inactivated JE vaccines propogated in mouse-brain tissues are available.

A live attenuated JEV vaccine is now the most widely used vaccine.


There have been reports of the JE in Pakistan (1983).

CHIKUNGUNYA (1)

Chikungunya fever is caused by a virus which belongs to the genus Alphavirus, in the family Togaviridae.

Chikungunya virus was first isolated from the blood of a febrile patient in Tanzania in 1953, and has since been cited as the cause of numerous human epidemics in many areas of Africa and Asia, and most recently in a limited area of Europe.

CHIKUNGUNYA (2)

Transmission:

Chikungunya virus is spread by the bite of an infected mosquito. Mosquitoes become infected when they feed on a person infected with chikungunya virus. Infected mosquitoes can then spread the virus to other humans when they bite. Monkeys, and possibly other wild animals, may also serve as reservoirs of the virus.

CHIKUNGUNYA (3)

Aedes aegypti (the yellow fever mosquito), an aggressive daytime biter which is attracted to humans, is the primary vector of chikungunya virus to humans. Aedes albopictus has also played a role in human transmission in Asia, Africa, and Europe. Various forest-dwelling mosquito species in Africa have been found to be infected with the virus.

CHIKUNGUNYA (4)

CHIKUNGUNYA (5)

Symptoms: Chikungunya virus infection can cause an illness,

characterized by fever, headache, fatigue, nausea, vomiting, muscle pain, rash, and joint pain. “Silent” chikungunya virus infections do occur. Chikungunya virus infection (whether clinically apparent or silent) is thought to confer life-long immunity. Acute chikungunya fever typically lasts a few days to a couple of weeks, but as with dengue, West Nile fever, o'nyong-nyong fever and other arboviral fevers, some patients have prolonged fatigue lasting several weeks.

CHIKUNGUNYA (6)


The best way to prevent chikungunya virus infection is to avoid mosquito bites. There is no vaccine or preventive drug currently available.

CHIKUNGUNYA (7)

Epidemiology:

The geographic range of the virus is primarily in Africa and Asia.

Given the current large chikungunya virus epidemics and the world wide distribution of Aedes aegypti and Aedes albopictus, there is a risk of importation of chikungunya virus into new areas by infected travelers.

CHIKUNGUNYA (8)

CHIKUNGUNYA (9)

THE END

Documents

E ASTERN M EDITERRANEAN A RBOVIRUSES Sogol Sheikh-Akbari