[afro-nets] Chikungunya Outbreaks

[Jawad Asghar <jawad@alumni.washington.edu>]

Chikungunya Outbreaks ­ The Globalization of Vectorborne
Diseases
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New Enland Journal of Medicine
Previous Volume 356:769-771, February 22, 2007, Number 8

Full text with photos available at:
http://content.nejm.org/cgi/content/full/356/8/769


Chikungunya Outbreaks ­ The Globalization of Vectorborne
Diseases

Rémi N. Charrel, M.D., Ph.D., Xavier de Lamballerie, M.D.,
Ph.D., and Didier Raoult, M.D., Ph.D.

In 2006, an outbreak of chikungunya fever ­ an arthralgic
disease caused by a mosquito-borne alphavirus ­ swept over a
number of islands in the Indian Ocean (the Comoros, Mauritius,
the Seychelles, Madagascar, Mayotte, and Reunion). In Reunion,
which has a population of 770,000, there were 265,000 clinical
cases (an incidence of 34%), and the disease was implicated in
237 deaths (about 1 per 1000 clinical cases); a recent report by
Reunion health authorities indicated that the seroprevalence was
35%, with very few asymptomatic cases. The epidemic had started
with outbreaks in Kenya in 2004 and the Comoros early in 2005.
More recently, it jumped to India, where there have been an
estimated 1.3 million cases to date.[1] When all is said and
done, the global toll of chikungunya in 2006 could be close to 2
million, and the disease may well continue to spread this year.

Sequence analysis of the virus genome revealed that this massive
outbreak was caused by a new variant.[2] Such changes are common
in viruses that have a positive-stranded RNA genome, because the
RNA-dependent RNA polymerase has no proofreading activity. A
mutation in the E1 envelope gene (A226V) has received special
attention, and some researchers have proposed that this mutation
may have modified the virus's ability to infect mosquitoes or
perhaps even the severity of the illness associated with human
infection. The mutation was reported to have occurred sometime
between the spring and the fall of 2005 ­ thus it cannot be
implicated in the early stages of the epidemic (the Kenyan and
Comorian outbreaks) but may be to blame for the adaptation to a
new mosquito vector.

In the Makonde language, "chikungunya" means "that which bends
up," and joint pains are a major feature of both the acute and
the chronic phases of the disease. The ankles and wrists are
most commonly involved; intense pain caused by pressure on the
wrist is a strong diagnostic sign of the disease.[2] Within 2 to
5 days of infection, conjunctivitis and a rash are common;
arthralgias can persist for weeks to months. Previously
undescribed severe clinical forms were reported in Reunion,
including cases caused by peripartum mother-to-infant
transmission and cases involving meningoencephalitis (sometimes
in newborns) and hepatic failure (although the liver damage may
have resulted from high doses of acetaminophen). Common
hematologic abnormalities in the acute phase include lymphopenia
and thrombocytopenia that may be associated with bleeding.
Levels of hepatic enzymes are commonly increased, and viral
loads are remarkably high ­ frequently above 109 virus particles
per milliliter of serum.

Chikungunya was diagnosed in an unprecedentedly large number of
people (more than 1000) who were returning to Europe and the
United States >from the areas where the outbreaks occurred. Such
infected people can disseminate the virus and initiate or fuel
new epidemics in countries where replication-competent vectors
reside, since no antiviral treatment is yet available. Also, as
a direct consequence of the high viremia in patients, direct
human-to-human transmission can occur, as was demonstrated in
southern France.[2]

In Kenya and the Comoros, the vector of the chikungunya virus
was Aedes aegypti, the vector previously reported to be involved
in transmission in Africa and Asia. In contrast, in Reunion and
Mauritius, A. albopictus, the Asian tiger mosquito, was the
primary vector. The devastating outbreak resulted from a
human­mosquito­human cycle that, as in dengue, did not require
an external nonhuman reservoir. A. albopictus is also prevalent
in Mayotte and Madagascar, but it is unclear which vector was
involved in most islands of the Comorian archipelago, where
studies have not been conducted or are ongoing. There is recent
evidence that the outbreak in India, where A. aegypti is the
primary species of mosquito, was caused by the new variant of
the virus.[3] A. albopictus is generally considered to have a
lower vector capacity for arboviruses than A. aegypti. Specific
mosquito populations, however, may have a high vector
capacity,[4] as suggested by a massive outbreak of dengue that
was propagated by A. albopictus in Reunion in 1977. It is also
possible that the strain of chikungunya virus in the Indian
Ocean became better adapted to the A. albopictus vector.

Introductions of nonnative species of plants, invertebrates, and
vertebrates are increasingly being recognized in countries with
temperate climates.[5] Among migrating invertebrate species,
mosquitoes that are capable of transmitting infectious diseases
are of particular interest. The expansion of global air travel
and seaborne trade removes geographic barriers to insect disease
vectors, enabling the insects to move great distances in short
periods. If they can adapt to the local environment, they
establish themselves in new areas. It is thus that mosquitoes of
the aedes (stegomyia) genus have gained an increasingly global
distribution. In the past 50 years, the anthropophilic A.
albopictus has spread to all continents (see map) and adapted to
most climates. Although long considered a secondary disease
vector, it has been shown to be capable of transmitting
arboviruses under both laboratory and field conditions.

Like epidemics of dengue and West Nile virus, the chikungunya
outbreak is an example of the abrupt expression of vectorborne
diseases in the global village. It involved an African virus and
an Asian mosquito and started in the Indian Ocean. The
establishment of new vectors makes possible the introduction of
new pathogens. Malaria, yellow fever, African tickborne
rickettsiosis, and more recently, West Nile virus have all been
imported from Africa to the Americas. After all, the spread of
such vectorborne diseases requires only a host reservoir and a
specific vector. If humans are the host reservoir and the vector
is widely distributed, globalization of the disease is just a
matter of time.

The emergence in 1999 of West Nile virus in the United States
and its subsequent rapid spread throughout the country
demonstrated that arboviruses can present a threat in developed
countries with temperate climates in the absence of herd
immunity. One can therefore justifiably speculate that the
chikungunya virus could establish itself in any tropical or
temperate area where A. albopictus is present today ­ or where
it migrates as its distribution continues to grow. Thus, the key
measures for preventing chikungunya epidemics include
entomologic surveillance, peridomestic mosquito control, public
education, detection of imported cases, and the early
recognition of local transmission followed by efficient vector
control.

Dr. Raoult reports that he is a cofounder of INODIAG, a
serologic diagnostics company.

Source Information

Drs. Charrel and de Lamballerie are professors in the Unité des
Virus Emergents, and Dr. Raoult a professor in the Unité des
Rickettsies, both in the Faculté de Médecine, Université de la
Méditerranée, Marseilles, France.

References

[1] Mudur G. Failure to control mosquitoes has led to two fever
epidemics in India. BMJ 2006;333:773-773. [Free Full Text]

[2] Parola P, de Lamballerie X, Jourdan J, et al. Novel
Chikungunya virus variant in travelers returning from Indian
Ocean islands. Emerg Infect Dis 2006;12:1493-1499.

[3] Yergolkar PN, Tandale BV, Arankalle VA, et al. Chikungunya
outbreaks caused by African genotype, India. Emerg Infect Dis
2006;12:1580-1583.

[3] Reiter P, Fontenille D, Paupy C. Aedes albopictus as an
epidemic vector of chikungunya virus: another emerging problem?
Lancet Infect Dis 2006;6:463-464.

[4] Shirley SM, Kark S. Amassing efforts against alien invasive
species in Europe. PLoS Biol 2006;4:e279-e279.

-- 
Rana Jawad Asghar MD. MPH.
Coordinator South Asian Public Health Forum
mailto:jawad@alumni.washington.edu
http://www.DrJawad.com Typhoid Net
http://www.typhoid.net