pro chikunguniya

A STUDY OF CHIKUANGUNYA
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Chikungunya fever is a viral disease transmitted to humans by the bite of infected
mosquitoes. Chikungunya virus was first isolated from the blood of a feverish
patient in Tanzania in 1953. It 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 is a viral fever caused by an alpha virus. The role of vector for the
spread of Chikungunya is played by Aedes aegypti mosquito. Aedes Aegypti is
also a vector for Dengue hemorrhagic disease. Chikungunya disease was first
detected and described in African continent by Marion Robinsonand W.H.R.
Lumsden in 1955 in Mekonde plateau near Tanganyika.
Since 2004, Chikungunya virus (CHIKV) has been causing large epidemics of
chikungunya fever (CHIK), with considerable morbidity and suffering. The

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epidemics have crossed international borders and seas, and the virus has been
introduced into at least 19 countries by travelers returning from affected areas.
Because the virus has been introduced into geographic locations where the
appropriate vectors are endemic, the disease could establish itself in new areas of
Europe and the Americas. The possibility that CHIKV could become established in
the Americas has heightened awareness of the need to develop guidelines for the
prevention and control of CHIK in PAHO’s Member Countries. This document is
meant to serve as a guideline that individual countries can use as the basis for their
CHIKV surveillance, prevention, and control programs.
History of Chikungunya
The disease was first detected in 1952 in Africa following an outbreak on the
Makonde Plateau. This is a border area between Mozambique and Tanzania. The
virus was isolated from the serum of a febrile patient from this area. The name
chikungunya is derived from the Makonde word meaning "thatwhich bendsup" in
reference to the stooped posturedeveloped as a result of the arthritic symptoms of
the disease. In Swahili this means "the illness of the bended walker”. Makonde is
the language spokenby the Makonde, an ethnic group in southeast Tanzania and
northern Mozambique.
According to the initial 1955 report about the epidemiology of the disease, the term
'chikungunya' is derived from the Makonde root verb kungunyala, meaning to dry
up or becomecontorted. The Makonde term was more specifically referred to as
"thatwhich bendsup". Subsequentauthors apparently overlooked the references to
the Makonde language and assumed that the term derived from Swahili, the lingua
franca of the region. The erroneous attribution of the term as a Swahili word has
been repeated in numerous print sources. Many other erroneous spellings and
forms of the term are in common use including "Chicken guinea", "Chicken
gunaya," and "Chickengunya".
Chikungunya virus (CHIKV) likely originated in Central/East Africa, where the
virus has been found to circulate in a sylvatic cycle between forest-dwelling
mosquitoes and nonhuman primates. In these areas, sporadic human cases occur,
but large human outbreaks were not common. However, in urban centers of Africa
as well as throughout Asia, the virus can circulate between mosquitoes and naive
human hosts in a cycle similar to that of dengue viruses.

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Since its discovery in Africa, in 1952, chikungunya virus outbreaks have occurred
occasionally, but recent outbreaks have spread the disease to other parts of the
world. Numerous chikungunya re-emergences have been documented in Africa,
Asia (India), and Europe, with irregular intervals of 2–20 years between outbreaks.
Currently, chikungunya fever has been identified in nearly 40 countries. In 2008,
chikungunya was listed as a US National Institute of Allergy and Infectious
Diseases (NIAID) category C priority pathogen.
A Phase II clinical vaccine trial, sponsored bythe US Government in 2000, used a
live, attenuated virus, developing viral resistance in 98% of those tested after 28
days and 85% still showed resistance after one year. However, live chikungunya
vaccines are still questionable as there could be a risk of a live vaccine possibly
inducing chronic rheumatism.
DNA vaccination is a technique for protecting an organism against disease by
injecting it with genetically engineered DNA to producean immunological
response. Nucleic acid vaccines are still experimental, and have been applied to a
number of viral, bacterial and parasitic models of disease, as well as to several
tumour models. DNA vaccines have a number of advantages over conventional
vaccines, including the ability to induce a wider range of immune responsetypes.
A recent study supports anovel consensus-basedapproachto vaccine design for
chikungunya virus employing a DNA vaccine strategy. The vaccine cassette was
designed based on chikungunya virus Capsid and Envelope specific consensus
sequences with several modifications, including codonoptimization, RNA
optimization, the addition of a Kozak sequence, and a substituted immunoglobulin
E leader sequence. Analysis of cellular immune responses, including epitope
mapping, demonstrates that these constructs induces both potent and broad cellular
immunity in mice. In addition, antibody ELISAs demonstrate that these synthetic
immunogens are capable of inducing high titer antibodies capable of recognizing
native antigen. Taken together, these results supportfurther study of the use of
consensus CHIKV antigens in a potential vaccine cocktail.

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OBJECTIVES:
General objectives are the prevention, detection, and timely responsethe outbreaks
of CHIK through surveillance, case detection, investigation, and the launching of
public health actions.

Signsand Symptoms
CHIKV can cause acute, subacute, and chronic disease. Acute disease is most often
characterized by suddenonset of high fever (typically greater than 102°F [39°C])
and severe joint pain.8−10 Other signs and symptoms may include headache,
diffuse backpain, myalgias, nausea, vomiting, polyarthritis, rash, and
conjunctivitis (Table 1).11 The acute phase of CHIK lasts for 3−10 days.
Chikungunya virus infection can cause a debilitating illness, most often
characterized by the following:
 fever
 headache
 fatigue
 nausea

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 vomiting
 muscle pain
 rash ,joint pain
Table1. Frequency of acute symptomsof CHIKV Infection
Symptom or sign frequency rate ( % of symptomaticpatient)
Fever 76−100
Polyarthralgias 71−100
Headache 17−74
Myalgias 46−72
Back pain 34−50
Nausea 50−69
Vomiting 4−59
Rash 28−77
Polyarthritis 12−32
Conjunctivitis 3−56
“Silent” chikungunya virus infections (infections without illness) do occur;but
how common they are is not yet known. 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 (diseases
that are caused by blood-sucking insects), some people have prolonged fatigue
lasting several weeks. Additionally, some people have reported incapacitating joint
pain, or arthritis, which may last for weeks or months.
Incubation period
The incubation period (time from infection to illness) can be 2–12 days, but is
usually 3–7 days.

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Causes
Chikungunya fever is caused by a virus which belongs to the genus Alphavirus,
family Togaviridae.
Types of Laboratory Tests Availableand SpecimensRequired
Three main types of laboratory tests are used for diagnosing CHIK: virus isolation,
reverse transcriptase-polymerase chain reaction (RT-PCR), and serology. Samples
collected during the first week after onset of symptoms should be tested by both
serological (immunoglobulin M [IgM] and G [IgG] ELISA) and virological (RT-
PCR and isolation) methods. Specimens are usually blood or serum, but in
neurological cases with meningoencephalitic features, cerebrospinal fluid (CSF)
may also be obtained. Limited information is available for the detection of virus by
isolation or RT-PCR from tissues or organs.
In suspected fatal cases, virus detection can be attempted on available specimens.
Selection of the appropriate laboratory test is based upon the source of the
specimen (human or field collected mosquitoes) and the time of sample collection
relative to symptom onset for humans.
Virus isolation
Virus isolation can be performed on field collected mosquitoes or acute serum
specimens (≤8 days). Serum obtained from whole blood collected during the first
week of illness and transported cold (between 2°−8°C or dry ice) as soonas
possible (within 48 hours) to the laboratory can be inoculated into a susceptible
cell line or suckling mouse. CHIKV will producetypical cytopathic effects (CPE)
within three days after inoculation in a variety of cell lines, including Vero, BHK-
21, and HeLa cells. Virus isolation can be performed in T-25 flasks or shell vials
(see Appendix A). Recent data suggest that isolation in shell vials is both more
sensitive and produces CPEearlier than conventional isolation in flasks.42 CHIKV
isolation must be confirmed either by immunofluorescence assay (IFA), using
CHIKV-specific antiserum, or by RT-PCR ofthe culture supernatant or mouse
brain suspension. Virus isolation must only be carried out in biosafety level 3
(BSL-3) laboratories to reduce the risk of viral transmission.

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RT-PCR
Several RT-PCR assays for the detection of CHIKV RNA have been published.
Real time, closed system assays should be utilized, due to their increased
sensitivity and lower risk of contamination. The Arboviral Diagnostic Laboratory
within DVBD, CDC routinely utilizes the published assay in Appendix B,43 which
demonstrates a sensitivity of less than 1 pfu or 50 genome copies. Serum from
whole blood is used for PCR testing as well as virus isolation.
Serological test
For serological diagnosis, serum obtained from whole blood is utilized in
enzymelinked immunosorbent assay (ELISA) and plaque reduction neutralization
testing (PRNT). The serum (or blood) specimen should be transported at 2°−8°C
and should not be frozen. Serologic diagnosis can be made by demonstration of
IgM antibodies specific for CHIKV or by a four-fold rise in PRNT titer in acute
and convalescent specimens. IgM antibodies specific for CHIKV are
demonstrated by using the IgM antibody capture ELISA (MAC-ELISA),44
followed by the PRNT (detailed protocols for IgM and IgG ELISAs shown in
Appendix C). As of 2010, there were no World Health Organization (WHO)
validated commercial IgM ELISAs available. PRNT is required to confirm the
MAC-ELISA results, since cross-reactivity in the MAC-ELISA between some
members of the Semliki Forestvirus (SFV) serogroup has been observed.
PRNT testing, whether used to confirm the MAC-ELISA or to demonstrate a four-
fold rise in acute/convalescent specimens, should always include other viruses
within the SFV serogroup (e.g., Mayaro virus) to validate specificity of reactivity.
In situations where the PRNT assay is not available, other serological tests (e.g.
hemaglutination inhibition [HI]) can be used to identify a recent alphavirus
infection; however, PRNT is required to confirm a recent CHIKV infection.

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An acute phase serum should be collected immediately after the onset of illness
and the convalescent phase serum 10−14 days later. CHIKV-specific IgM and
neutralizing antibodies normally develop towards the end of the first week of
illness. Therefore, to definitively rule out the diagnosis, convalescent samples
should be obtained on patients whose acute samples test negative.
MATERIALS AND METHODS
Cell culture and Viruses
C6/36 mosquito cell line was maintained at 37°C under 5% CO2 by regular sub
culturing at periodic intervals of 4 to 5 days in Mitsuhashi and Maramorosch's
medium. CHIKV are grown in <48 hours old suckling mice and also in C6/36
mosquito cell culture was used as viral antigen positive standard in the assay
systems employed in the present study. Briefly, the monolayer of C6/36 cells
grown in 25-cm2 culture flask was adsorbed with 0.5 ml of the inoculum at 37°C
for 2 h. Following adsorption, the inoculum was replenished with 10 ml of
maintenance medium supplemented with 2% fetal bovine serum. Suitable mock-
infected cell controls were also kept. The cells were then incubated at 37°C and
observed daily for cytopathic effects . Upon observation of 80 to 100% cytopathic
effects, the infected culture supernatant was clarified by light centrifugation at
2,000 rpm for 10 min and further purified by sucrosedensity gradient
ultracentrifugation according to standard protocols. The brain suspensions from
mice infected with the virus were the sourceof antigen . Approval for use of mice

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for antigen preparation was obtained from the institutional ethical committee
according to national guidelines.
Clinical Specimens
A total of 40 acute-phase serum samples received from patients with a clinical
diagnosis of Chikungunya fever were used for evaluation in this study. The acute-
phase samples were collected during the period between 1 and 7 days after the
onset of symptoms. All the samples were stored at -80°C until further
investigation.
In addition, a panel of 10 serum samples collected from healthy individuals was
also included as negative controls.
Virus titration and isolation
The haemagglutination activity of the arbovirus is pH dependent. Therefore it is
necessary to titrate the antigen at different pH. This is useful to determine the pH
for the antigen dilution to be used 9. The antigen was vortexed and 100El added in
the first well as marked in the plate. Two-fold dilution was made by transferring
50El from the first well of each column. The final 50El is then discarded. 50El of
0.4% Red Blood Cells (RBC) suspension prepared in the respective VAD to the
corresponding well was added. First add to the control wells and then to the
antigen containing well. Manually it was mixed by agitating the plates thoroughtly.
It was incubated at 370C for 1 h.
Diagnosis
Preliminary diagnosis is often based on clinical features, places and dates of travel
(if the personis from a non-endemic country or area), activities, and epidemiologic
history of the location where infection occurred.

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Laboratory diagnosis of arboviral infections is generally accomplished by testing
the blood or cerebrospinal fluid, or CSF (the fluid that surrounds the brain and
spinal column) to detect virus-specific antibodies.
During an acute infection, certain viruses can be isolated through culture or
detected by nucleic acid amplification, or PCR (a technique that makes multiple
copies of the viral genetic material, making it easier to detect).
In fatal cases, nucleic acid amplification (PCR), histopathology using
immunohistochemistry (a technique that uses antibodies to identify proteins in
diseased cells), and virus culture of autopsy tissues can also be useful. Only a few
state laboratories or other specialized laboratories, including those at the Centers
for Disease Control and Prevention (CDC), are capable of doing this specialized
testing.
Treatment
Treatment is symptomatic and can include rest, fluids, and medicines to relieve
symptoms of fever and aching. Medicines such as ibuprofen, naproxen,
acetaminophen, or paracetamol can help relieve pain and fever.
Aspirin should be avoided. During the first few days of illness, infected persons
need to be protected from further mosquito exposure by staying indoors in areas
with screens and/or under a mosquito net. This is so that they do not contribute to
the transmission cycle, which leads to further infection of other people.
Treatmentfor ChikungunyaArthritis
A bout of chikungunya fever can severely affect the joints of the body. Resulting
pain can last for up to a year, if not attended to in time. However, in most patients
the pain recedes in about 2 weeks. Those diagnosed with chikungunya arthritis,
suffer a lot of pain and it also affects their mobility. There is a wide variety of
available treatments for the same.
Allopathic Treatment for Chikungunya Arthritis
Chikungunya arthritis cannot be treated with the mere use of drugs like Asprin.
 A 250 mg daily dosage of Chloroquine Phosphate has been proven to be apt
treatment for chikungunya arthritis in many cases. The drug acts as an anti-
inflammatory agent and relieves crippling pain.

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 Research has also suggested that the use of the drug Ribavirin has also been
successful in treating chikungunya arthritis. The drug effectively eases the
pain in the ankles and other joints in most cases.
 Another allopathic method of treating chikungunya arthritis is long term
anti-inflammatory therapy that helps in reducing pain.
Ayurvedic Treatment for Chikungunya Arthritis
Ayurveda is supposed to be extremely beneficial in subduing chikungunya arthritic
pain.
 The best known ayurvedic drug for treating chikungunya arthritis is
Arthoven. It has herbal properties and ingredients such as Dashamoola and
Punarnava which are effective in reducing the swelling of joints and ease
pain.
 There are also many ayurvedic massages and therapies that help in boosting
the immunity of the body. A healthy immunity system then attacks the viral
antigens that are both directly and indirectly related to chikungunya arthritis.
 Ayurveda also suggests some rejuvenation medicines and therapies that
positively influence an individual suffering from chikungunya arthritis. It
helps them fight against the ailment and lead a healthy life.
Although there is no exact cure for treating chikungunya arthritis, its symptoms
can be effectively controlled with the help of medicines and a healthy diet. It is

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important to lead a healthy lifestyle so that the pain related with chikungunya
arthritis can be kept in check.
How to Treat Chikungunya Fever
Chikungunya is an insect-borne viral disease that is transmitted to humans by the
virus-carrying Aedes mosquitoes. This fever is self-limiting and resolves with the
passage of time .i.e. most patients of chikungunya fully recover from virus
infection overtime. Drinking lots of water and taking plenty of rest can also help in
reducing the pain and suffering.
Medication for Chikungunya
The World Health Organization has not prescribed any vaccine or drug for treating
chikungunya till now. Since there is no acceptable treatment in allopathic
medicine; aspirin, combiflam, ibuprofen and paracetamol are been largely used by
doctors for reducing the associated pain and fever.
Supportive therapies such as administration of non-steroidal and anti-inflammatory
drugs tend to ease the symptoms. Some patients show positive response to these
medications while the others don’t. One cannot totally rely on medication when it
comes to treating chikungunya fever.
Mild exercises and regular body movement also tend to improve morning
arthralgia (joint pain) and stiffness.

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Ayurvedic Treatment for Chikungunya
Ayurvedic methods are doing wonders in treating chikungunya fever. In ayurveda
the patient’s body is provided with necessary resistance for combating the disease.
Herbs that bring relief to the symptoms of chikungunya fever include:
 Triphala-is a good medicine for Chikungunya. It is an ayurvedic
composition of three fruits namely Harada, Amla and Behada.
 Grapes- dry and seedless grapes when taken with cow’s milk bring relief to
severe symptoms of chikungunya.
 Carrot- when taken in raw form, carrot increases the resistance of the
person suffering from chikungunya.
 Sacred Basil (Tulsi)- basil leaves are effective in reducing the fever.
 Sunflower seeds- sunflower seeds when taken with honey is a good
supplement for chikungunya patients.
Other effective ayurvedic preparations include sudarshan choorna and yogiraj
guggulu. Many people question effectiveness of ayurvedic medicines for complete
treatment of chikungunya but the herbs surely are effective in controlling severe
symptoms.
Homeopathic treatment for Chikungunya
Homeopathy offers many medicines that can be helpful in Chikungunya. Some of
them include:
 Eupatorium-perf
 Pyroginum
 Rhus-tox
 Cedron
 Influenzinum
 Arnica
 Belladona
 Bryonia
Amongst the above stated medicines, Eupatorium-perf is considered to be a
preventive medicine for Chikungunya. Homeopathic medicines can reduce the

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intensity and treat nagging joint pains. The potency of the medicines depends on
the intensity of the fever and the symptoms.
Chloroquine:
Chloroquine is conventionally used drug in clinical practice for the treatment of
Malaria. It
has specific role in Rheumatoid arthritis patients where it works as disease
modifying anti rheumatic drug. It has been found to have a similar kind of
immune-modulatory role in the
management of Chikungunya. Chlorine atom attached to position 7 constitutes
greatest anti malarial activity .
The Toxicity of Chloroquine is reduced in form of hydroxyl Chloroquine and its
analogues which are used for therapy of conditions other than malaria .This
alkaloid concentrates itself in lysosomes and has anti inflammatory properties .
Thus these compounds often with other agents have effects on Rheumatoid
Arthritis , SLE Systemic Lupus erythematosis , Sarcoidosis photosensitivity
diseases such as Porphyrea Cutanea Tarda.
This study was carried out during epidemic of chikungunya in a private practice
clinic set up.
The recent outbreak of Chikungunya fever in the twin cities of Hyderabad and
Secunderabad, India was declared by W.H.O in the month of December 2005.
Currently
there is no specific treatment protocolfor Chikungunya. The purposeof this study
was to
prove the efficacy of Chloroquine in the management of Chikungunya.
During the Chikungunya epidemic outbreak in the month of June 2006,
Chloroquine phosphatewas administered to the patients diagnosed with the
condition in the form of
injectable/ per oral tablet/ syrup. A total of 193 cases were seen during the period
of 3 months from the month of June 2006 to August 2006, out of the 193 cases of
Chikungunya 90 patients were males 103 females. All these cases were diagnosed
on the basis of signs and symptoms associated with Chikungunya like fever, severe
arthritis resulting in inability to ambulate. The
improvement in the pain was studied using visual analogue scale while adverse
events were studied by Noranjo algorithm scale . Every day 10mg per kg
Chloroquine given for adults and 5 mg/kg for children. No Chloroquine injections
below 5 years and precautionary use in children above 5 years of age and below 10

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years . During the fever period Paracetomol 2 gms per day was given for 3 to 5
days during the first 7 days.
Chloroquine Phosphateis one of the oldest drug in market with proven safety.
Most important finding in this study is efficient management of Chikungunya
which has high morbidity. It’s immune-modulatory role has been proved by in
vitro prophylactic and therapeutic efficacy of Chloroquine against Chikungunya
virus in VeroChloroquine Phosphatecan be used in the treatment of Chikungunya.
During the acute phase of first 3 days involving fever it can be combined with
Paracetemol for 3-5 days and then only Chloroquine tablets could be
continued for 7 days. Chloroquine is the drug already in use, and well known not to
have any adverse effects even when it is used up to 3 months in 250 mgs dosages
in cases of rheumatoid arthritis.
The particular conclusions about this study is remarkable patient improvement
with Chloroquine almost completely in most patients on VAS scale .
Chloroquine is already proved disease modifying anti-Rheumatoid arthritis drug .
There are also studies which have assessed invitro prophylactic and therapeutic
efficacy of chloroquine against chikungunya virus in vero cells2 based on this I can
conclude that there is a huge role for Chloroquine in the management of
Chikungunya .
Safety of Chloroquine:
Safety of Chloroquine has been established since time immemorial in the use as an
antimalarial drug. Chloroquine phosphate is considered safe during pregnancy and
in children. Safety of Chloroquine was studied by Norenjo scale where it stands at
1 to 4.
Prevention
The bestway to prevent chikungunya virus infection is to avoid mosquito bites.
There is no vaccine or preventive drug currently available. Prevention tips are
similar to those for other viral diseases transmitted by mosquitoes, suchas dengue
or West Nile. The following can help avoid mosquito bites:
 Using insect repellent containing DEET, Picaridin, oil of lemon eucalyptus,
or IR3535 on exposed skin.
 Wearing long sleeves and pants (ideally treat clothes with permethrin or
another repellent)
 Having secure screens on windows and doors to keep mosquitoes out

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 Getting rid of mosquito sources in the yard by emptying standing water from
flower pots, buckets, and barrels
 Changing the water in pet dishes and replacing the water in bird baths
weekly Drilling holes in tire swings so water drains out
 Keeping children's wading pools empty and turned on their sides when they
aren't being used
Additionally, a personwith chikungunya fever can reduce the risk of spreading the
fever by limiting exposure to mosquito bites. Mosquito repellents help discourage
mosquito bites, as does limiting exposure to mosquitoes (by staying indoors or
using screens or mosquito nets).
How Chikungunya isSpread
Humans become infected with chikungunya virus by the bite of an infected
mosquito. Aedes aegypti, a household container breeder and aggressive daytime
biter is the primary vector of chikungunya virus to humans. The Asian tiger
mosquito (Aedes albopictus)has also played a role in human transmission is Asia,
Africa, and Europe. Various forest-dwelling mosquito species in Africa have been
found to be infected with the virus.
Basicviral transmission cycle
Mosquitoes become infected with chikungunya virus when they feed on an
infected person. The infection is spread when the mosquito bites another person.
Monkeys, and possibly other wild animals, may also serve as reservoirs of the
virus.
Expected Outcome
Fatalities related to chikungunya virus are rare and appear to be associated with
increased age.
Epidemiology
CHIKV is an RNA virus that belongs to the Alphavirus genus in the family
Togaviridae. The name chikungunya derives from a word in Makonde, the
language spoken by the Makonde ethnic group living in southeast Tanzania and

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northern Mozambique. It roughly means “that which bends,” describing the
stooped appearanceof persons suffering with the characteristic painful arthralgia.
Recent Outbreaks
After the initial identification of CHIKV, sporadic outbreaks continued to occur,
but little activity was reported after the mid-1980s. In 2004, however, an outbreak
originating on the coastof Kenya subsequently spread to Comoros, La Réunion,
and several other Indian Ocean islands in the following two years.
From the spring of 2004 to the summer of 2006, an estimated 500,000 cases had
occurred.
The epidemic spread from the Indian Ocean islands to India, where large outbreaks
occurred in 2006. Once introduced in India, CHIKV spread to 17 of the country’s
28 states, infecting more than 1.39 million people before the end of the year. The
outbreak in India continued into 2010, with new cases appearing in areas that had
not been affected in the epidemic’s early phase. Viremic travelers also spread
outbreaks from India to the Andaman and Nicobar Islands, Sri Lanka, the
Maldives, Singapore, Malaysia, Indonesia. Concern over the spread of CHIKV
peaked in 2007, when the virus was found to be spreading autochthonously
(human-to-mosquito-to-human) in northern Italy after being introduced by a
viremic traveler returning from India.4 The attack rates in communities that have
been affected in the recent epidemics ranged from 38%−63%, and in many of these
countries cases continue to be reported, albeit at reduced levels. In 2010, the virus
continued to cause illness in India, Indonesia, Myanmar, Thailand, and the
Maldives; it also has resurged in La Réunion. In 2010, imported cases also were
identified in Taiwan, France, and the United States. These cases were infected
viremic travelers returning from Indonesia, La Réunion, and India, respectively.
During the recent outbreaks, individuals viremic with CHIKV were found in the
Caribbean (Martinique), the United States, and French Guiana.5 All of them had
returned from areas with endemic or epidemic CHIKV transmission; thus, these
cases were not due to autochthonous transmission. All of these areas have
competent mosquito vectors and naïve hosts, however, and thus could support
endemic transmission of CHIKV in the Americas. Given these factors, CHIKV has
the capacity to emerge, re-emerge, and quickly spread in novel areas, which
makes heightened surveillance and preparedness a priority.
Epidemics of fever, rash, and arthritis resembling CHIK were reported as early as
the 1770s. However, the virus was not isolated from human serum and mosquitoes
until an epidemic in Tanzania in 1952−1953.1 Subsequent outbreaks occurred in
Africa and Asia, many of them affecting small or rural communities.

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In Asia, however, CHIKV strains were isolated during large urban outbreaks in
Bangkok, Thailand, in the 1960s and in Calcutta and Vellore, India, during the
1960s and 1970s.
Entomological study of chikungunyainfections in the State of Kelantan, Malaysia
Entomological study of chikungunya infections in the State of Kelantan,
MalaysiaSince its first report in 19531, chikungunya has caused numerous massive
outbreaks worldwide. Asia was reported to have the first outbreak in Bangkok in
19582 and later in Cambodia, Vietnam, Laos, Myanmar, Malaysia, the Philippines
and Indonesia3. In Malaysia the disease was first reported in Klang, Selangor
between 1998 and February 19994 and reemerged in Bagan Panchor, Perak in
20065. In April 2008, another
Background & objectives:
Chikungunya infection has becomea public health threat in Malaysia since the
2008 nationwide outbreaks. Aedes albopictus Skuse has been identified as the
chikungunya vector in Johor State during the outbreaks. In 2009, several outbreaks
had been reported in the State of Kelantan. Entomological studies were conducted
in Kelantan in four districts, namely Jeli, Tumpat, Pasir Mas and Tanah Merah to
identify the vector responsible for the virus transmission.
Methods: CHIKV cases records were obtained from State Health Department,
Kelantan and localities involved were identified. Larva survey was conducted to
collect the immature mosquito stages. Modified aspirators were used to collect the
adult mosquitoes. All samples on dry ice were transferred to laboratory and the
presence of the virus was detected using reverse transcriptase PCR.
Results: A total of 1,245 mosquito larvae were collected during larval survey and
2,019 adult mosquitoes were collected using aspirator. From these collections, 640
mosquito pools were tested for the presence of CHIKV by RT-PCR butnone found
positive. Ae. albopictus was the most abundant mosquito collected, followed by
Culex sp., Armigeres sp. and Anopheles sp. A total of 2, 814 artificial containers
were inspected during the study.

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Interpretation & conclusions: Since none of the mosquito samples was found to be
positive for chikungunya virus, the vector(s) of chikungunya virus in these
localities could not be identified.
Since its first report in 19531, chikungunya has caused numerous massive
outbreaks worldwide. Asia was reported to have the first outbreak in Bangkok in
19582 and later in Cambodia, Vietnam, Laos, Myanmar, Malaysia, the Philippines
and Indonesia3. In Malaysia the disease was first reported in Klang, Selangor
between 1998 and February 19994 and reemerged in Bagan Panchor, Perak in
20065. In April 2008, another outbreak occurred in Johor State which then spread
to other States and federal territories in Malaysia.
Chikungunya virus (CHIKV) has been known as enzootic in many countries in
Asia and Africa, transmitted by various wild Aedes mosquitoes and has been
isolated from different mosquito species. Aedes aegypti and Aedes albopictus are
usually considered as potential vectors of CHIKV since they have been proven
susceptible to this virus in many laboratory studies. Ae. albopictusSkuse has been
detected with chikungunya virus in Ipoh, Perak State in 200610. In 2009, several
outbreaks had been reported in the State of Kelantan11, the borderState between
Malaysia and Thailand. In order to identify the vector(s) responsible for the
outbreaks in Kelantan State, we conducted several entomological investigations in
Kelantan between June to December 2009.
Material & Methods
Studysites: Based on reported cases by State Health Department, Kelantan, a
survey was conducted between June to December 2009 in localities with cases of
chikungunya in four districts, namely Jeli, Tumpat, Pasir Mas and Tanah Merah.
Mosquito collection: Larva survey was conducted to collect the immature
mosquitoes based on the recommended method12. All indoor and outdoor
containers that were potential breeding sites were inspected, whereas adult
collection was conducted using sweep net and modified aspirator. Collection
started between 0800-1200 h and 1500-1800 h between June to December 2009
one day after cases being notified by the District Health Department.
Mosquito processing: All mosquito samples were pooled on dry ice according to
species, sex and type of breeding containers in sterile 2.0 ml plastic tubes, with

Page 20
maximum of 30 individuals per pooland transported to Medical Entomology Unit,
Institute for Medical Research laboratory in dry ice.
Virus detection by reverse transcriptase polymerase chain reaction: The
mosquitoes were ground in the tubes with 1 ml of maintenance medium (Eagle’s
minimum essential medium, MEM)9, using a sterile homogenizer and the RNA
was extracted using QIAamp Viral RNA Mini Kit (Qiagen, Germany) according to
manufacturer’s protocol. Forpositive control, equal volume of cultured cells
infected with chikungunya virus was used while for negative control, uninfected
cultured cells were used. The RT PCR assay was conducted using the Titan One
Tube RT-PCR kit (Roche, Germany), adapted from the methods by Hasebe et al13.
Amplified productwas analyzed by gel electrophoresis and all positive samples
was confirmed by sequencing the amplicons.
Result& Discussion
Through the disease epidemiology study done simultaneously in the localities, a
total of 70 patients were confirmed infected with chikungunya virus. This indicated
that the transmission was still active in the localities. Using modified aspirator and
sweep net, a total of 3,264 mosquitoes (1245 larvae, 2019 adult) were collected
(Table I) which comprised 57.9 per cent Aedes albopictus, 37.46 per cent Culex sp,
4.6 per cent Armigeres sp and 0.03 per cent of Anopheles sp in four different
districts in Kelantan during the study. Aedes albopictus was found to be the
predominant species collected. However, Ae. aegypti was not found during the
survey, which might indicate that Ae. albopictus was the main breeder in artificial
breeding containers available in the localities.
Although Ae. aegypti has been considered to be the principal vector, Ae. albopictus
was repeatedly shown to be a competent vector of CHIKV during recent outbreaks
in Indian Ocean, Italy, Gabon, and even in Malaysia. This virus was also detected
from field collected Ae. albopictusin Madagascar during 2006 outbreak.
This is believed to be associated with CHIKV with a mutation in envelope protein
gene (E1-A226V) which enabled the CHIKV to adapt to Ae. albopictus. A total of
640 mosquito pools were tested during the study. Virus detection by RT-PCR
showed that none of the pools were positive, however, the positive controls
confirmed that the PCR tests worked well. Therefore, our study was not able to
clarify the role of Ae. albopictus, Ae. aegypti or other mosquitoes species as vector
transmitting chikungunya virus at the studied localities. The possibility of other

Page 21
mosquitoes in transmitting the virus needs to be taken into consideration since
chikungunya virus has reportedly been transmitted.
The virus primarily inhabits Africa and Asia. Given the current large chikungunya
virus epidemics and the world wide distribution of Aedes aegypti and Aedes
albopictus, the virus could be imported to new areas by infected travelers.
Outbreaks
Below is a list of some chikungunya outbreaks:
 Tanzania in 1953-1954 (first recorded outbreak)
 Kolkata, India in 1963
 27 people in Port Klang, Malaysia, in 1999
 237 deaths and 33% of people infected in Réunion in 2006 and 2007
 160 people in Italy in 2007
 43,138 people in Kerala in 2007
 Melborne, Australia in 2008
Pregnancyand Chikungunya
Pregnant women can become infected with chikungunya virus during all stages of
pregnancy and have symptoms similar to other individuals. Most infections will
not result in the virus being transmitted to the fetus. The highest risk for infection
of the fetus/child occurs when a woman has recently been infected and has the
virus in her blood at the time of delivery. There are also rare reports of first
trimester (0–14 weeks) abortions occurring after chikungunya infection. Mosquito
repellants containing DEET can be used in pregnancy without adverse effects.
Breastfeeding and Chikungunya
Currently, there is no evidence that the virus is transmitted through breast milk.
Research
The first animal model of Chikungunya infection was developed in 2008. The
model allows researchers to study infection in greater detail, and thus guide future
drug and vaccine treatments. For the model, mice are genetically engineered to
have a deficiency in a gene that encodes a protein involved in the immune system

Page 22
responseto viral infection. The model has already showed that the virus replicates
in the liver before infecting skin, joints, and muscles. The central nervous system
becomes involved in the most serious infections
MANAGEMENT GUIDELINES FOR CHIKUNGUNYA
Introduction
Chikungunya fever (CF) is a vector borne viral illness. The disease was
documented first time in Tanzania in 1952-1953.


Agent
Chikungunya fever is caused by a single stranded, heat labile RNA virus that
belongs to the Alphavirus genus of the Togaviridae, the family that comprises a
number of viruses that are mostly transmitted by arthropods.

Vector
Aedes aegypti is the common vector responsible for transmission in urban areas
whereas Aedes albopictus has been implicated in rural areas. The adult female
mosquito rests in cooland shady areas in domestic and peri-domestic settings and
bites during day time.
Reservoirs
During inter-epidemic periods, a number of vertebrates have been implicated as
reservoirs. These include monkeys, rodents, birds, and other vertebrates. The exact
nature of the reservoir status in South-East Asia Region has not been documented.
Environment
Outbreaks are most likely to occurin post-monsoonperiod when the vector density
is very high. Human beings serve as Chikungunya virus reservoir during epidemic
periods.
There is no significant sex predilection and the virus causes illness in almost all
age groups.

Page 23
Management Clinical Feature
• Fever (92%)
The fever varies from low grade to high grade, lasting for 24 to 48 hours. Fever
rises abruptly in some, reaching 102-1040F (39-400C), with shaking chills and
rigor and usually subsides with use of antipyretics. No diurnal variation was
observed for the fever.
• Arthralgia (87%),
Many patients presented with arthralgia without fever. The joint pain tends to be
worse in the morning, relieved by mild exercise and exacerbated by aggressive
movements. The pain may remit for 2-3 days and then reappear in a saddle back
pattern. Migratory polyarthritis with effusions may be seen in around 70% cases,
but resolves in the majority. Ankles, wrists and small joints of the hand were the
worst affected. Larger joints like knee and shoulder and spine were also involved.
There is a tendency for early and more significant involvement of joints with some
trauma or degeneration. Occupations with predominant overuse of smaller joints
predisposed thoseareas to be affected more. (eg. interphalangeal joints in rubber
tappers, ankle joints in those standing and walking for a long time e.g., policemen).
The classical bending phenomenon was probably due to the lower limb and back
involvement which forced the patient to stoop downand bend forward.
• Backache (67%) and
• Headache (62%)
• Rash
Incubation period: 2-4 days
Sequelae
Persistent arthralgia
Complete resolution in 87.9 %
Episodic stiffness and pain
Persistent stiffness without pain and
Persistent painful restriction of joint movements.
Enthesopathy and tendinitis of tendoachilles
Neurological, emotional and dermatologic sequelae are also described.

Page 24
Differential diagnosis
Leptospirosis
Dengue fever
Malaria
Meningitis
Rheumatic fever
Clinicalmanagement
There is no specific antiviral drug against CHIK virus and treatment is entirely
symptomatic
Paracetamol (up to two 500 mg tablets four times daily), is the drug of choice
with use of other analgesics if paracetamol does not provide relief
During the acute stage of the disease, steroids are not usually indicated because
of the adverse effects.
Aspirin is preferably avoided for fear of gastrointestinal and other side effects
like Reye’s syndrome.
Mild forms of exercise and physiotherapy are recommended in recovering
persons.
Treatment should be instituted in all suspectcases without waiting for serological
or viral confirmation.
All suspected cases should be kept under mosquito nets during the febrile period.
Communities in the affected areas should be sensitized about the mosquito
control measures to be adopted in hospital premises and houses.
Cold compresses may help in reducing joint damage
Consumeplenty of water with electrolytes (approximately 2 litres of home
available fluids with salt in 24 hours). If possible ensure a measured urine output of
more than a litre in 24 hours.
Refrain from exertion. Mild forms of exercise and physiotherapy are
recommended in recovering persons.
Adequate rest in a warm environment; avoid damp surroundings. Heat may
increase/worsen joint pain and is therefore bestto avoid during acute stage.

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Laboratory Investigation
For treating Chikungunya fever laboratory testing for chikungunya is not
encouraged, physicians are requested to not going for laboratory confirmation
The confirmation of Chikungunya fever is through any of the followings:
• Isolation of virus
• PCR
• Detection of IgM antibody
• Demonstration of rising titre of IgG antibody
IgM antibodies demonstrable by ELISA may appear within two weeks. It may not
be advisable to do the antibody test in the first week. In some persons it may take
six to twelve weeks for the IgM antibodies to appear in sufficient concentration to
be picked up in ELISA
Leucopenia with lymphocyte predominance is the usual observation.
Erythrocyte sedimentation rate is usually elevated.
C-Reactive Protein is increased during the acute phase and may remain elevated
for a few weeks.
Control and Prevention:
Minimizingvector population
Remove stagnant water from all junk items lying around in the household and in
the peri domestic areas
Stagnating water in flower pots or similar containers should be changed daily or
at least twice weekly.
Introducelarvivorous fish in aquaria, garden pools, etc
Weeds and tall grasses should be cut short to minimize shady spaces where the
adult insects hide and rest during hot daylight hours
Drain all water stagnating after rains
Fogging and street sanitation with proper waste management (fogging does not
appear to be effective, yet it is routinely implemented in epidemic situation
Minimizethe vector-patientcontact
At household level:
o Have the patient rest under bed-nets, preferably permethrin impregnated nets
o Have infants in the house sleep under similar bed nets

Page 26
o Insecticide sprays: bed rooms, closets and crevices, bathrooms, kitchens, nooks
and corners;alternatively, coils, mats etc
o Have the patient as well as other members of the household wear full sleeves to
cover extremities, preferably bright coloured clothes
o Wire-mesh/ nets on doors and windows
Risk communicationto the household members
Educate the patient and other members in the household about the risk of
transmission to others and the ways to minimize the risk by minimizing vector
population and minimizing the contact with vector
Chikungunya fever: clinical manifestations & management
The recent epidemics of Chikungunya fever and the return of dengue fever in India
reflect the tenacity and survival capability of mosquitoes that continue to be man’s
deadliest foes. Chikungunya fever caused by Chikungunya virus (family
Togaviridae, genus Alphavirus) is transmitted by the bite of infected Aedes aegypti
and Aedes albopictus mosquitoes (that also transmit dengue and yellow fevers)4,5.
Historical accounts of epidemics of fever, arthralgias/arthritis and rash, resembling
what we now call as “Chikungunya fever” have been recorded as early as 1824 in
India and elsewhere.
In modern times, Chikungunya fever was first described in 1952 , following an
outbreak on the Makonde Plateau, along the borderbetween Tanganyika and
Mozambique. The word “Chikungunya” translates to “that which bends up” in

Page 27
reference to the stooped posturedeveloped due to the rheumatological
manifestations of the disease. Fora long time, it was erroneously reported both in
reputed medical journals9 as well as in lay press and the media that the word
“Chikungunya” was derived from the “Swahili” language. However, it has been
suggested that the word “Chikungunya” is derived from the Makondelanguage,
spoken by an ethnic group in southeast Tanzania and northern Mozambique from
the root verb “kungunyala”, meaning “to dry up or becomecontorted”, and
signifies the cause of a contortion or folding.
Chikungunya fever epidemics are characterized by explosive outbreaks
interspersed by periods of disappearance that may last from several years to a few
decades. A complex interaction between various factors such as the susceptibility
of humans and the mosquito vectors to the virus; conditions facilitating mosquito
breeding resulting in a high vector density, ability of the vector to efficiently
transmit the virus, all are thought to play a role. Increasing globalization can also
facilitate the introduction of the virus from other endemic areas (e.g., international
travel) . The natural cycle of the virus is human-mosquito-human.
We donotknow how the virus is maintained in the wild in Asia. Unlike dengue
virus, there is no evidence for transovarial transmission of Chikungunya virus in
mosquitoes. Variations in the geographical strains of Aedes mosquitoes regarding
their susceptibility to infection and ability to transmit the virus may be crucial
factors in determining endemicity of Chikungunya virus in a given region.
Vertical maternal-foetal transmission has been documented in pregnant women
affected by Chikungunya fever.
Following the report from Tanganyika in 1952 , Chikungunya epidemics have
been reported from
several countries in Africa, Asia, and else where. In Asia, epidemics have been
documented in India, Sri
Lanka, Myanmar, Thailand, Indonesia, the Philippines, Cambodia, Vietnam, Hong
Kong and Malaysia. Since 2003, there have been outbreaks in the islands of the
Pacific Ocean, including Madagascar, Comoros, Mayotte the Seychelles, and
Mauritius. The outbreak which began in 2005 in Reunion Island (French overseas
district in the Indian Ocean) is currently ongoing.
Since the first Indian report from Kolkata (Calcutta then) in 1963, several
outbreaks of Chikungunya fever have been documented from different parts of

Page 28
India including Vellore, Chennai (then called Madras) and Pondicherry in Tamil
Nadu, Visakhapatnam, Rajahmundry, and Kakinada in Andhra Pradesh, Nagpur
and Barsi in Maharastra. Occasional cases were recorded in Maharastra State
between 1983 and 2000. Keeping with the character of the disease, it reemerged
after nearly 32 yr in October2005. Phylogenic analysis based on partial sequences
of NS4 and E1 genes showed that the current isolates were African genotype
while all earlier isolates (1963-1973) were Asian genotype. As on October28,
2006, 1364135 cases suspected to be Chikungunya fever have been recorded from
several parts of the country, which is now showing a downward trend.
Chikungunya fever affects all age groups and both sexes are equally affected. The
incubation period ranges from 3-12 days (usually 3-7 days). In susceptible
populations, Chikungunya fever can have attack rates as high as 40 to 85 per cent.
The onset is usually abrupt and sudden with high grade fever (usually 102-105 oF),
severe arthralgias, myalgias and skin rash. Prodromal symptoms are rarely
reported.
During the initial few days, headache, throat discomfort, abdominal pain and
constipation are also frequent.
There is conjunctival suffusion, persistent conjunctivitis, and cervical or sometimes
generalized
lymphadenopathy, with maculopapular or petechial rash present usually on the
extremities, neck trunk and ear lobes. Swollen tender joints and crippling arthritis
is usually evident. The viral polyarthropathy frequently involves the small joints of
the hand, wrist and ankles and may also involve the larger joints such as knee and
shoulder. The pain may be severe enough to immobilise the patient and interfere
with sleeping in the night. Rheumatological manifestations are some what less
frequent in children.
Paediatric subjects may also experience febrile seizures, vomiting, abdominal pain
and constipation. Unlike dengue fever, haemorrhagic manifestations are
uncommon in Chikungunya fever. When present, they are mild and are more
frequently encountered in Asian compared with African patients. These
manifestations include epistaxis, bleeding from the gums, positive Hess test,
subconjunctival bleed and petechial/purpuric rash.
Rarely meningoencephalitis has also been described. The fever is of short duration
and usually resolves in three to four days. In some patients, a biphasic pattern of
fever has been described with a febrile episode of four to six days, followed by a
fever free period of a few days followed by recurrence of fever (usually 101-102

Page 29
oF) that may last a few days. Chikungunya is a self limiting disease, and the joint
pains resolve in one to three weeks. However, in about 12 per cent of the patients,
arthritis persisting for up to three years after the onset of illness has been
documented.
Indiscriminate use of corticosteroids, nonsteroidal anti-inflammatory drugs
(NSAIDS), especially aspirin and antibiotics can contribute to thrombocytopenia,
gastrointestinal bleeding, nausea, vomiting and gastritis. This may lead to
dehydration, pre-renal acute renal failure, dyselectrolytemia, and sometimes
hypoglycaemia. These can indirectly contribute to the mortality due to
Chikungunya fever.
In our experience at the Sri Venkateswara Institute of Medical Sciences, Tirupati, a
tertiary care referral centre, in Andhra Pradesh, (n=876 Chikungunya suspects)
during the period January-September 2006, short abrupt onset fever (100%), severe
and crippling arthritis, most frequently involving knees, ankles, wrists, hands, and
feet (98%) have been the most significant clinical manifestations. Rare
manifestations included meningoencephalitis (1%), fulminant hepatitis (2%).
Haemorrhagic manifestations were also relatively uncommon (3%) and have been
mild when present (unpublished data).
Various conditions from which Chikungunya fever must be distinguished from
other viral haemorrhagic fevers and viral fevers presenting with arthritis and skin
rash such as dengue fever, West Nile fever, O’nyong-nyong fever, Sindbis fever;
other common problems such as falciparum malaria and leptospirosis. Twin
outbreaks of dengue fever and Chikungunya fever are known to occurfrequently,
as it is happening in several parts of India presently, especially in Andhra Pradesh
and it becomes particularly important to distinguish one from the other. In a study
published from Thailand26, it was reported that, compared with patients with
dengue haemorrhagic fever, subjects with Chikungunya were more likely to
manifest arthralgia/arthritis, maculopaular rash and conjunctival injection.
However, laboratory testing is essential to distinguish Chikungunya fever from the
other conditions. In endemic areas, like for example, at our centre at Tirupati, even
during the peak of the Chikungunya fever epidemic, and the resurgence of dengue
fever, there has been no respite from the load of falciparum malaria and
leptospirosis.
The gold standard for the diagnosis of Chikungunya fever is viral culture, which is
seldom routinely done due to lack of adequate facilities. It has the advantage of

Page 30
detecting a wide range of viruses. Reverse transcriptionpolymerase chain reaction
(RT-PCR)has also been found to be a useful molecular tool for the rapid
diagnosis. More frequently, serodiagnostic methods for the detection of IgM and
IgG antibodies against Chikungunya virus in acute and convalescent sera are used.
These include indirect immunofluorescent method (IIF), enzyme linked
immunosorbent assay (ELISA), haemagglutination inhibition or neutralization
techniques.
Treatment of Chikungunya fever is symptomatic and supportive. Ensuring
adequate fluid intake, judicious use of paracetamol or NSAIDS for symptom relief
can be helpful. Aspirin should be avoided due to its effect on platelets. Some
clinicians have used hydroxychloroquine/chloroquine for treating the viral
arthropathy of Chikungunya fever.
Published evidence does not supportthe use of corticosteroids, antibiotics or
antiviral drugs in the management of Chikungunya fever and indiscriminate use of
these agents can be hazardous.
Electrolyte imbalance, pre-renal acute renal failure, bleeding manifestations should
be watched for carefully and managed accordingly. Patients with Chikungunya
fever should be advised to avoid being bitten by mosquitoes as the disease can be
transmitted to others. Thus, the role of educating the community and public health
officials, and adequate vector controlmeasures at the individual and community
levels cannnot be over emphasized.
Future requirements
Several areas on Chikungunya fever that merit future research include (i) the
reason(s) for mysterious behaviour of dramatic outbreaks interspersed by periods
of prolonged absence; (ii) development of an effective vaccine; (iii) affordable,
reliable and reproducible indigenously developed, rapid serodiagnostic useful in
the field setting; and (iv) a nationwide network of reliable, high quality of virology
laboratories and developing a surveillance system for monitoring outbreaks of
Chikungunya, dengue and other diseases.
A drastic change in the outlook of the community and public health authorities
with regard to hygiene and mosquito control measures is essential to stand a
chance in the war against the mosquitoes.

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Susceptibilityand Immunity
All individuals not previously infected with CHIKV (naïve individuals) are at risk
of acquiring infection and developing disease. It is believed that once exposed to
CHIKV, individuals will develop long lasting immunity that will protectthem
against reinfection.
Chikungunya CaseStudy (Sarosini Devi)
Name : Sarosini Devi a/p R.Kandiah
Age : 60 years old
Gender : Female
She came down with high fever for 4 days on late October2008 and was
suspected of Chikungunya fever by Hospital Universiti Kebangsaan Malaysia
(HUKM).
She was weak and not able to walk properly because of the pain. She developed
inflammation on her shoulders as well as on her wrist. Her condition worsened as
she lost her appetite, too.
On 17th of November 2008, she was given MAS AYU products, namely Mas Ayu
Amirtha, Mas Ayu Semalu and Mas Ayu Aki, which were administered 1 capsule
per productfor 3 times a day.
Only after 4 days of MAS AYU nutritional treatment all her swelling had subsided.
She could walk properly and the pain on the joints subsided as well. Her general
health improved tremendously.
Mas Ayu Amirtha:
1. Regulation of the biochemical and physiological balance of the body.
2. Improves the quality and quantity of blood.

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3. Optimizes immunity and maintains a disease refusal state.
Mas Ayu Semalu:
1. Natural mild antibiotic.
2. Adjunct for viral fever.
Mas Ayu Aki:
1. Improves energy, stamina and strength.
2. Improves metabolism of absorbed foods.
3. Regulation of carbohydrate metabolism
Burden of chikungunya in India
Background & objectives: During 2006, chikungunya emerged as a major ever
known epidemic in India. Disability adjusted life years (DALY) is an appropriate
summary measure of population health to express epidemiological burden of
diseases. We estimated the burden due to suspected chikungunya using DALYs for
the first time and compared between the states and also with the burden due to
other vector-borne diseases in India. The economic burden was also assessed in
terms of productivity loss.
Methods: Data on the reported cases of fever/suspected cases of chikungunya
from different states during 2006 in India were used. Years lived with disability
(YLD) were calculated for non-fatal cases to estimate DALY. Since the disability
weight for chikungunya is not available, the weights available for rheumatic
arthritis, comparable to the disease outcome of chikungunya were used for the
estimation. The burden was estimated for both acute and chronic cases. It is
considered that about 11.5% of cases were reported to have extended morbidity
with persisting arthralgia. For acute disease, the average duration of illness was
considered to be nine days and for chronic cases it was six months on an average.
The productivity loss due to income foregone by the working class was calculated
using minimum official wage.

Page 33
Results National burden of chikungunya was estimated to be 25,588 DALYs
lost during 2006
epidemic, with an overall burden of 45.26 DALYs per million. It varied from 0.01
to 265.62 per
million in different states. Karnataka alone contributed as high as 55% of the
national burden.
Persistent arthralgia was found to impose heavy burden, accounting for 69% of the
total DALYs.
The productivity loss in terms of income foregone was estimated to be a minimum
of Rs. 391
million. Chikungunya affected at least 213 districts in 15 states in India during the
year 2006.

Page 34
Table 1. Basic model of DALY estimation with values for various input
parameters
Parameter Base value Range
Source (Reference)
Multiplication factor 1 1.96–4.45
24
Disability weight 0.233 0.233–0.81
25, 26
Duration of illness (acute days) 9 1–30
24, 30
Duration of disability chronic (days) 6 months 6 months –3 year
5, 31
Proportion of persistent arthralgia 0.12 0.11–0.69
5, 34
Positivity rate (%) for chikungunya 100 2.7–100
14
district wise details were not available and the whole state population was
considered
as under risk. The total population at risk of infection was 565.41 million and the
number of fever/suspected chikungunya cases were as high as 1.39 million and
ranged between 35 (Lakshadweep) and 7,62,026 (Karnataka). The overall
incidence per thousand population was calculated to be 2.46 and itranged between
0.04 (NCT of Delhi) and 14.45 (Karnataka) The number of blood samples
screened for chikungunya varied between 6 and 5421 from different states and the
positivity rate ranged from 2.7 (Goa) to 100% (West Bengal and Lakshadweep).
Out of the total 15,504 samples screened, 12.8% were positive for chikungunya.
When corrected to the sero-positivity rate, out of 1.39 million at least 0.148 million
cases were definitely
Interpretation & conclusion:The chikungunya epidemic in the year 2006
imposed heavy epidemiological burden and productivity loss to the community.
The burden of chikungunya in terms of DALY was estimated for the first time. In

Page 35
view of re-emergence and spread of this infection in recent times it is warranted for
derivation of disability weight for different health states of chikungunya to
facilitate realistic estimates of DALYs. Quality epidemiological data from
surveillance system to monitor vector-borne and zoonotic diseases would pave way
for more realistic estimates of burden. The productivity loss in-terms of income
foregone could be minimal as the estimation was made by using the minimum
wage fixed by the government although the actual loss is expected to be higher.
ECONOMIC IMPACT OF CHIKUNGUNYA EPIDEMIC: OUT-OF POCKET
HEALTH EXPENDITURES DURING THE 2007 OUTBREAK IN KERALA,
INDIA
The southern state of Kerala, India was seriously affected by a chikungunya
epidemic in 2007. As this outbreak was the first of its kind, the morbidity incurred
by the epidemic was a challenge to the state’s public health system. A cross
sectional survey was conducted in five districts of Kerala that were seriously
affected by the epidemic, using a two-stage cluster sampling technique to select
households, and the patients were identified using a syndromic case definition.
We calculated the direct health expenditure of families and checked whether it
exceed the margins of catastrophic health expenditure (CHE). The median (IQR)
total out-of-pocket(OOP) health expenditure in the study population was USD7.4
(16.7). The OOP health expenditure did not show any significant association with
increasing per-capita monthly income.The major share (47.4%) of the costs was
utilized for buying medicines, but costs for transportation (17.2%), consultations
(16.6%), and diagnoses (9.9%) also contributed significantly to the total OOP
health expenditure. The OOP health expenditure was high in private sector
facilities, especially in tertiary care hospitals. For more than 15% of the
respondents, the OOP was more than double their average monthly family
income.The chikungunya outbreak of 2007 had significantly contributed to the
OOP expenditure of the affected community in Kerala.The OOP health
expenditure incurred was high, irrespective of the level of income. Governments
should attempt to ensure comprehensive financial protection by covering the costs
of care, along with loss of productivity.

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Quantifying the Impactof Chikungunya and Dengue on Tourism Revenues
Background
Health economists have traditionally quantified the burden of vector-borne
diseases (such as
chikungunya and dengue) as the sum of the costof illness and the costof
intervention programmes.
The objective of this paper is to predict the order of magnitude of possible
reduction in tourism
revenues if a major epidemic of chikungunya or dengue were to discourage visits
by international tourists, and to prove that even a conservative estimate can be
comparable to or even greater than the costof illness and intervention programmes
combined, and therefore should not be ignored in the estimation of the overall
burden.
Methods
We have chosenthree Asian economies where the immediate costs ofthese
diseases have been
recently calculated: Gujarat (an economically important state of India), Malaysia,
and Thailand.
Only international tourists from non-endemic countries have been considered to be
discouraged, and a 4% annual decline in their numbers has been assumed.
Revenues from these tourists have been calculated assuming that tourists from non-
endemic countries would spend, on average, the same amount as all international
tourists. These assumptions are conservative and consistent with the recent
experience of Mauritius and Réunion islands. Non-Resident Indians (NRIs) have
been
considered half as likely to avoid travel to Gujarat compared to non-Indians. This
paper reports
inflation-adjusted expenditure figures as 2008 US$, assuming recent market
exchange rates of 42.0 INR/US$, 3.22 MYR/US$, 0.68 EUR/US$, and 33.6
THB/US$.
Findings
A 4% decline in tourists from non-endemic countries would result in a substantial
loss of tourism
revenues – at least US$ 8 million for Gujarat, US$ 65 million for Malaysia, and
US$ 363 million for Thailand. The estimated immediate annual costof
chikungunya and dengue to these economies is US$ 90 million, US$ 133 million,

Page 37
and approximately US$ 127 million respectively, indicating that impact on tourism
revenues should not be ignored when calculating the burden of infectious diseases.
The impact on Gujarat is relatively less because its share of world tourism receipts
is just 0.04%,
whereas Malaysia and Thailand have healthy shares of 1.64% and 1.82%
respectively. A 4% decline in tourists to Gujarat from other Indian states would
amount to US$ 9.6 million loss in domestic tourism revenues to Gujarat.
Interpretation
The potential loss of tourism revenues due to a severe epidemic outbreak could be
substantial. In some cases, ignoring this component could seriously underestimate
cost-benefit results, forestalling promising interventions that could benefit the
society as a whole or leading to inadequate investment of resources in prevention
and public-funded control programmes. This would be to the detriment of
especially poorer sections of the society, who may not be able to afford treatment
costs. At present data are insufficient for us to make more than a preliminary
estimate of the magnitude of the potential loss of revenues from tourism due to a
major outbreak of chikungunya or dengue.
GUIDELINES ON CLINICAL MANAGEMENTOF CHIKUNGUNYA FEVER (W.H.O.)
Clinical Management of CF is discussed at two stages (1)Acute stage of the
illness and (2) Sequelae.
• There is no specific antiviral drug against CHIK virus
• Treatment is entirely symptomatic
• Paracetamol is the drug of choice with use of other analgesics if paracetamol does
not provide relief
• During the acute stage of the disease, steroids are not usually indicated because of
the adverse effects.
• Aspirin is preferably avoided for fear of gastrointestinal and other side effects
like Reye’s syndrome.
• Mild forms of exercise and physiotherapy are recommended in recovering
persons.

Page 38
• Treatment should be instituted in all suspectcases without waiting for serological
or viral confirmation.
• During an epidemic, it is not imperative that all cases should be subjected for
virologic/serologic investigations.
• All suspected cases should be kept under mosquito nets during the febrile period.
• Communities in the affected areas should be sensitized about the mosquito
control measures to be adopted in hospital premises and houses.
Guidingprinciplesfor managing acutestage
Clinical Management of CF during acute stage can be elaborated at four levels
• Domiciliary (Home care)
• At the primary level or point of first contact ( PHC/CHC level)
• At the secondarylevel (District Hospital)
• At the tertiary level (Teaching hospital situations / infectious
diseasesspecialists/advanced care centres.)
Domiciliary(Home based)
All cases of fever cared in their own homes should be advised on the following.
• Adequate rest in a warm environment; avoid damp surroundings. Heat may
increase/worsen joint pain and is therefore bestto avoid during acute stage.
• Refrain from exertion. Mild forms of exercise and physiotherapy are
recommended in recovering persons.
• Cold compresses may help in reducing joint damage

Page 39
• Consume plenty of water with electrolytes (approximately 2 litres of home
available fluids with salt in 24 hours). If possible ensure a measured urine output of
more than a litre in 24 hours.
• Take paracetamol tablets during periods of fever (up to two 500 mg tablets four
times daily), in persons with no preexisting liver or kidney disease
• Avoid self medication with aspirin or other pain killers.
When to seek medical help?
• Fever persisting for more than five days
• Intractable pain
• Postural dizziness, cold extremities
• Decreased urine output
• Any bleeding under the skin or through any orifice
• Incessant vomiting
At the point of first contact (PHC/CHC level)
All fever cases must be seen by a medical officer and differential diagnoses of
dengue fever, leptospirosis, malaria and other illnesses excluded by history,
clinical examination and basic laboratory investigations.
All persons should be assessed fordehydration and properrehydration therapy
(preferably oral) instituted quickly.
Severe dehydration is characterized by two of these signs:
• abnormal sensorium, excessive sleepiness or lethargy
• sunken eyes
• poorfluid intake
• dry, parched tongue
• reduced skin turgor (very slow skin pinch taking more than 2 sec to retract)
Mild or Moderate dehydration is characterized by two of these signs:
• restlessness or irritability
• sunken eyes
• dry tongue
• excessive thirst
• slow skin pinch (less than 2 seconds to retract)

Page 40
Collect blood samples for total leucocyte count, platelet count. The total leucocyte
count is usually on the lower side (below 5000 cells / cu. mm). If it is more than 10
000 per cu mm, the possibility of leptospirosis has to be considered. A low platelet
count (below 50 000 per cu. mm) should alert the possibility of dengue fever. The
peripheral smear has to be examined for malarial
parasite as well and if positive, treatment started as per national guidelines.
Treat symptomatically (Paracetamol 1g three to four times a day for fever,
headache and pain, antihistamines for itching). Paracetamol must be used with
caution in persons with preexisting underlying serious illnesses. Children may be
given 50-60 mg per kg bodyweight per day in divided doses. Tepid sponging can
be suggested.
If the casehas already been treated with paracetamol/ other analgesics, start one of
the NSAIDS (as per standard recommendations). Monitor for any adverse side
effects of NSAIDS. Cutaneous manifestations can be managed with topical or
systemic drugs.
If the personhas hemodynamic instability (frequent syncopalattacks, hypotension
with a systolic BP less than 100 mmHg or a pulse pressure less than 30 mmHg),
oliguria (urine output less than 500 ml in 24 hours), altered sensorium or bleeding
manifestations, refer immediately to a higher healthcare centre. Refer persons not
responding or having persistent joint pain or disabling
arthritis even after three days of symptomatic treatment. It may be advisable to
refer persons above sixty years and infants (below one year of age) as well. Heat
may increase/worsen joint pain and is therefore best to avoid during acute stage.
Mild forms of exercise and physiotherapy are recommended in recovering persons.
Patients may be encouraged to walk, use their hands for eating, writing and regular
isotonic exercises. Cold compresses may be suggested depending on the response.
Exposure to warm environments (morning and evening sun) may be suggested as
the acute phase subsides.
At the secondary level (district hospital)
All fever cases with joint or skin manifestations must be evaluated by a physician.
Assess for dehydration and institute proper rehydration therapy, preferably by oral
route (as above) Collect blood samples for serology (IgM – ELISA). As an
alternative, blood test for IgG may be done — to be followed by a second sample
after two to four weeks.
Investigate the person for renal failure (urine output, serum creatinine, serum
sodium and potassium), hepatic insufficiency (serum aminotransferases, bilirubin),

Page 41
cardiac illness (ECG), malaria (peripheral smear study), and thrombocytopenia.
Consider CSF study if meningitis is suspected.
If the casehas already been treated with paracetamol/ other analgesics, start an
NSAID (as per standard recommendations). Monitor for adverse effects from
NSAID use. Cutaneous manifestations can be managed with topical or systemic
drugs.
Refer cases with any of the following to a higher healthcare centre: pregnancy,
oliguria/anuria, refractory hypotension, bleeding disorders, altered sensorium,
meningoencephalitis, persistent fever of more than one week’s duration, and
extremes of age - persons above sixty years and infants (below one year of age).
CURB 65 scoring system may be used for deciding on referrals.
Encourage activities and advise regarding complications. Exercises like walking on
level grounds, active hand movements and proper posturing of joints to avoid
contractures must be suggested. Instruct about the activities mentioned above for
further home care.
If a serologic test for IgG was done, remember to draw a second blood sample after
a gap of 2-4 weeks.
At the tertiary care level (Teaching hospitalsituations/infectious diseases
specialists/advanced care centres)
In cases referred to tertiary care centre,
• Ensure that all above-mentioned processes have been completed.
• Collect blood samples for serology/PCR/ genetic studies as early as possible, if
facilities are available.
• Consider the possibility of other rheumatic diseases like rheumatoid arthritis
(with the criteria for rheumatoid arthritis diagnosis being fulfilled), gout, rheumatic
fever (with modified Jones’ criteria) etc.. in unusual cases. Institute therapy with
NSAIDS.
CURB-65 is a clinical prediction rule that has been validated for predicting
mortality in community-acquired pneumonia and infection of any site.
The scoreis an acronym for each of the risk factors measured. Each risk factor
scores one point, for a maximum scoreof 5:
• Confusion
• Urea greater than 7 mmol/l (Blood Urea Nitrogen > 19)
• Respiratory rate of 30 breaths per minute or greater
• Blood pressureless than 90 systolic or diastolic blood pressure 60 or less • age 65
or older

Page 42
• Treat serious complications (bleeding disorders with blood components-platelet
transfusions in case of bleeding with platelet counts of less than 50,000 cells per cu
mm., fresh frozen plasma, or
Vitamin K injections if prothrombin time INR is more than 2, hypotension with
fluids/ inotropics, acute renal failure with dialysis, contractures and deformities
with physiotherapy/surgery, cutaneous manifestations with topical or systemic
drugs, and neuropsychiatric problems with specialist care and drugs). Patients with
myopericarditis or meningoencephalitis may require intensive care with regular
monitoring, inotropic support, ventilation etc. In cases with ophthalmic
complications, standard practice guidelines may be obtained from the
ophthalmologists.
• Use hydroxychloroquine 200 mg orally once daily or chloroquin phosphate 300
mg orally per day for a period of four weeks in cases where arthralgia is refractory
to other drugs. Before using chloroquine or related compounds in these doses, the
peripheral blood smear examination must be done at least twice to rule out malaria.
• If one IgG test only was done earlier, remember to draw a second blood sample
after a gap of 2-4 weeks.
• Assess the disability and recommend rehabilitative procedures.
Guidingprinciplesfor managing chronicphase
Managementof osteoarticular problems
The osteoarticular problems seen with Chikungunya fever usually subside in one to
two weeks’ time. In approximately 20% cases, they disappear after a gap of
few weeks. In less than 10% cases, they tend to persist for months. In about 10 %
cases, the swelling disappears; the pain subsides, but only to reappear with every
other febrile illness for many months. Each time the same joints get swollen, with
mild effusion and symptoms persist for a week or two after subsidenceof the fever.
Complement mediated damage and persistence of the virus in intracellular
sanctuaries have been implicated in occasional studies. Destroyed metatarsal head
has been observed in patients with persistent joint swelling.
Management of osteoarticular manifestations follow the general guidelines given
earlier. Since an immunologic etiology is suspected in chronic cases, a short course
of steroids may be useful. Care must be taken to monitor all adverse events and the
drug should not be continued indefinitely to prevent adverse effects. Even though
NSAIDS producesymptomatic relief in majority of individuals, care should be
taken to avoid renal, gastrointestinal, cardiac and marrow toxicity. Cold
compresses have been reported to lessen the joint symptoms.
Disability due to Chikungunya fever arthritis can be assessed and monitored using
one of the standard scales. As discussed above, properand timely physiotherapy
will help patients with contractures and deformities. Nonweight bearing exercises

Page 43
may be suggested.; e. g. slowly touching the occiput(back of the head) with the
palm, slow ankle exercises, pulley assisted exercises, milder forms of yoga etc.
Surgery may be indicated in severe and disabling contractures. The management
plan may be finalized in major hospitals, but the follow-up and long-term care
must be done at a domiciliary or primary health centre level.
Occupational assistance after detailed disability assessment needs to be provided.
Managementof neurological problems
Various neurologic sequelae can occurwith persistent chikungunya fever.
Approximately 40% of those with CF will complain of various neurological
symptoms but hardly 10% will have persistent manifestations. Peripheral
neuropathy with a predominant sensorycomponent is the most common (5- 8%).
Paresethesias, pins and needles sensations, crawling of worms sensation and
disturbing neuralgias have all been described by the patients in isolation or in
combination. Worsening or precipitation of entrapment syndromes like carpal
tunnel syndrome has been reported in many patients. Motor neuropathy is rare.
Occasional cases of ascending polyneuritis have been observed as a postinfective
phenomenon, as seen with many viral illnesses. Seizures and loss of consciousness
have been described occasionally, but a causal relationship is yet to be found. Anti-
neuralgic drugs (Amitryptyline, Carbamazepine, Gabapentin, and Pregnable) may
be used in standard doses in disturbing neuropathies.
Ocular involvement during the acute phase in less than 0.5% cases as described
above may lead to defective vision and painful eye in a small percentage.
Progressive defects in vision due to uveitis or retinitis may warrant treatment with
steroids.
Managementof dermatological problems
The skin manifestations of Chikungunya fever subsideafter the acute phase is over
and rarely require long term care. However worsening of psoriatic lesions and
atopic lesions may require specific management by a qualified specialist.
Hyperpigmentation and papular eruptions may be managed with Zinc oxide cream
and/or Calamine lotion. Persistent non-healing ulcers are rare. Scrotaland
aphthous- like ulcers on the skin and intertriginous areas may be managed by
saline compresses, and topical or systemic antibiotics if secondarily infected.

Page 44
Managementof psycho-somatic problems
Neuro-psychiatric / emotional problems have been observed in upto 15% cases.
These are more likely in persons with pre-morbid disorders and those with a family
history of mood disorders. They may take different forms.
The emotional and psychosocial issues need individual assessment and have to be
considered in the social context of the patient and community.
Often patients have inadequate information regarding Chikungunya. Broadly,
psychosocialsupportand reassurance may solve some of the problems. A well
thought about plan for community support, occupationaland social rehabilitation
may hold the key for success.
State-wise status of chikungunya fever in india,2005
CONCLUSION:
Chikungunya virus belongs to the family of alphaviruses and is common in
Southeast Asia and Africa. It can be transmitted to humans by bites of the Aedes
mosquitoes. Symptoms are similar to those of dengue and consistof fever,
headache, arthralgia, myalgia and conjunctivitis. After two or three days these
symptoms subside and a maculopapular rash appears. The fever may return.

Page 45
Arthralgia can persist over weeks and even months. While the diagnosis is
normally established by antibody tests, these may be negative in early stages of the
disease. when the diagnosis can be made by PCR. Treatment is symptomatic with
analgesics and antipyretics.

Page 46
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