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| Last Updated:: 12/01/2012


Chikungunya virus out breaks in Andhra Pradesh, Karnataka and Maharashtra

Chikungunya (CHIK) virus, a member of the Alphavirus genus, was first isolated from the serum of a febrile human in Tanganyika (Tanzania) in 1953 (Karabatsos, 1985). It is a relatively rare form of viral fever spread by bites from Aedes aegypti mosquito.This virus is closely related to O'nyong'nyong virus and it is not a fatal disease.

CHIK virus originated in Africa and which was subsequently introduced into Asia, where it is now typically associated with Ae. aegypti mosquitoes. CHIK in Asia has been documented since 1958 in Bangkok. Between 1960s and 1980s, this virus was isolated from numerous countries of Asia, Central and Southern Africa. Since 1953, CHIK virus has caused numerous well-documented outbreaks and epidemics in both Africa and SouthEast Asia, involving hundreds of thousands of people (Halstead et al., 1969a,b; Rao, 1966). The clinical symptoms of CHIK infection often mimic those of dengue fever because this virus circulates in regions where dengue virus is endemic. It has been postulated that many cases of dengue virus infection are misdiagnosed (Carey, 1971). Several other togaviruses of the alphavirus genus (Ross River, O’nyong-nyong, etc) have also been associated with a similar syndrome.

About Chikungunya virus:

The alphaviruses are enveloped particles and their genome consists of a single-stranded, positive-sense RNA molecule of approximately 12000 nucleotides. The 5' end is capped with a 7-methylguanosine while the 3' end is polyadenylated. The non-structural proteins are translated directly from the 5' of the genomic RNA. A subgenomic positive-strand RNA referred to as 26S RNA, identical to the 3' of the genomic RNA, is transcribed from a negative-stranded RNA intermediate. This RNA serves as the mRNA for the synthesis of the viral structural proteins (Strauss & Strauss,1986,1988; Faragher et al.,1988). According to the genomic organization of other alphaviruses, the genome of CHIK is considered to be: 5' cap-nsP1-nsP2-nsP3-nsP4-(junction region)-C-E3-E2-6K-E1-poly(A) 3'.

Bionomics of Aedes aegypti:

Aedes is a genus of mosquito found in tropical and subtropical zones. This mosquito has become a significant pest in many communities because it closely associates with humans (rather than living in wetlands), and typically flies and feeds in the daytime rather than at night or at dusk and dawn. Morphologically, this mosquito shows distinct patterns in white lines, a lyre-shaped line on the sides of the thorax and the palps are half white. The proboscis is generally all black in color. Ae. aegypti feeds throughout the day with peaks of activity at mid-morning and late afternoon. It is a container and puddle breeder, needing only a few ounces of fresh water to breed. Eggs can withstand dessication. It has a short flight range (less than 200 m).

Seasonal variation in population density and distribution is common for Ae. aegypti since it is sensitive to changes in temperature and available moisture. Essentially, low mosquito populations are evident in dry and cool seasons and they increase when temperatures increase and the wet season commences (Schultz, 1993). Cement tanks are found to be the primary containers for Aedes breeding because water in these containers never empty and replenish periodically, making them the perennial breeding sites. Besides other containers like clay jars, drums, coolers and ornamental plant bottles are also found to be positive for Aedes breeding. During the onset of monsoons these places serve as potential breeding sites for Ae. aegypti and Ae. albopictus. A survey report says that, breeding places of Ae. aegypti accounts nearly 39% in large water holding sites like drums and water storage jars, 44% in mid-sized containers like rock holes, buckets and tires while highest 48% in all other small containers.




Seasonal factors influence the breeding sites that regulates the Ae. aegypti population. Mostly humans are responsible for providing suitable breeding sites for these mosquitoes by ignoring the stagnant water bodies in and around the locality. Hence, existence of this species throughout the year is probably due to the arid climate and subsequent behavior by local residents. The mosquito is endophagic that prefers to feed in and around structures and then rests in cool damp spots within structures. A blood meal takes 2-7 days to digest and 1-3 meals are needed to complete development of clutch of eggs. Transmission among humans occurs from repeated biting when the mosquito injects saliva that acts as an anticoagulant.

Clinical Symptoms:
CHIK is an acute infection of abrupt onset, heralded by fever and severe arthralgia, followed by other constitutional symptoms and rash and lasting for a period of 1-7 days. The incubation period is usually 2-3 days, with a range of 1-12 days. After incubation period fever rises abruptly, often reaching 390C to 400C and is accompanied by intermittent shaking chills. This acute phase lasts 2-3 days. The temperature may remit for 1-2 days, resulting in a "saddle-back" fever curve.
The arthralgias are polyarticular, migratory, and predominantly affect the small joints of the hands, wrists, ankles and feet, with lesser involvement of larger joints. Pain in joints exacerbated by strenous exercise can be decreased by mild exercise. Joint swelling occurs due to accumulation of fluid. Patients with milder articular manifestations are usually symptom-free within a few weeks, but more severe cases require months to resolve entirely. Generalized myalgia as well as back and shoulder pain, is common.
Cutaneous manifestations are typical with many patients presenting with a flush over the face and trunk. This is usually followed by a rash generally described as maculopapular. The trunks and limbs are commonly involved, but face, palms and soles may also show lesions. Pruritis or irritation may accompany the eruption.
During the acute disease, most patients will have headache. Photophobia and retro-orbital pain also occur in moderation. In infants and younger children, prominent flushing and early appearance of maculopapular or urticarial eruption may be a useful indicator and they also display neurological symptoms.
Supportive care with rest is indicated during the acute joint symptoms. Movement and mild exercise tend to improve stiffness and morning arthralgia but heavy exercise may exacerbate rheumatic symptoms. In unresolved arthritis refractory to aspirin and nonsteroidal antiinflammatory drugs, chloroquine phosphate (250 mg/day) has given promising results.

The definitive diagnosis can only be made by laboratory means, but CHIK should be suspected when epidemic disease occurs with the characteristic triad of fever, rash and rheumatic manifestations.
Virus isolation is readily accomplished by inoculation of mosquito cell culture, mammalian cell culture or suckling mice. Viremia will be present in most patients during the first 48 hours of disease and may be detected as late as day 4 in some patients.
Detection of antigens or antibody to the agent in the blood (serology).
ELISA is available.
An IgM capture ELISA is necessary to distinguish the disease from dengue fever.

Recent outbreaks

In India:

Karnataka, Andhra Pradesh and Maharashtra have been severely affected by the disease this year. There have been reports of large scale outbreak of CHIK virus in Southern India. At least 80,000 people in Gulbarga, Tumkur, Bidar, Raichur, Bellary, Chitradurga, Davanagere, Kolar and Bijapur districts in Karnataka state are known to be affected since December 2005 to May, 2006.
In early part of 2006, there was a big outbreak in the Andhra Pradesh state in India. Nearly 200,000 people were affected by this disease in the districts of Praksham and Nellore. Some deaths have been reported but it was thought to be mainly due to the inappropriate use of antibiotics and anti-inflammatory tablets. As this virus can cause thrombocytopenia, injudicious use of these drugs can cause erosions in the gastric epithelium leading to exsangunating upper GI bleed (due to thrombocytopenia).

Chikungunya out break in Kerala-2007
Chikungunya out break in Kerala-2007
Chikungunya out break in West Bengal
Chikungunya nesessitating new insights-2009

A mixed outbreak of Chikungunya, with sporadic cases of dengue has also been reported in Andhra Pradesh state, India. During 1st December 2005 - 17th February 2006, 5671 cases of fever with arthralgia are reported. High density of Aedes aegypti were also reported in these areas. From 1st-15th March, over 2000 cases of Chikungunya have been reported from Malegaon town in Nasik district, Maharashtra state, India. In Orissa state, India, 4904 cases of fever associated with myalgia
and headache have been reported during 27th February - 5th March 2006. These signs are consistent with an arbovirus outbreak.

World wide:

In February 2005, an outbreak was recorded on the French island of Réunion in the Indian Ocean. As of February 25, 2006, 1,57,000 residents have been hit by the virus in the past year (out of a population of about 777,000 - 20% were affected). Since October 2005, 52 deaths have been associated with Chikungunya (French health minister Xavier Bertrand said that 77 deaths in January 2006 may have been "directly or indirectly attributable" to the outbreak. France initiated a massive effort to eradicate mosquitos' nesting grounds involving over 4000 people, including 800 troops.In neighboring Mauritius, 3,500 islanders have been hit in 2005. There have also been cases in Madagascar, Mayotte and the Seychelles.
 Chikungunya out break in Italy

Ann M. Powers, Aaron C. Brault, Robert B. Tesh and Scott C. Weaver: Re-emergence of chikungunya and o’nyong-nyong viruses: evidence for distinct.geographical lineages and distant evolutionary relationships. Journal of General Virology (2000), 81, 471-479.