Chikungunya virus

CHIKUNGUNYA
 Also known as Chicken Guinea
 It is a mosquito borne viral disease caused by Chikungunya virus viral
infection spread by the mosquitoes of genus Aedes
1. Aedes Aegypti,
2. Aedes Albopictus (Tiger mosquito).
 Chikungunya comes from the word “kungunyala” in Makonde language which
means “that which bends up” or “contoured”
 The person affected with Chikungunya walks with a stooped posture due to the
joints pain

Aggressive daytime-biting mosquitoes
highly-infective.
It is possible for a person to have chikungunya and dengue
fever together at the same time because the infected aedes
mosquito can carry both the viruses.

What Happens in Chikungunya?
Acute Phase
 Incubation period is usually 2 to 6 days
 Abrupt onset of fever with joint pains and stiffness, especially at beginning of motion
 Temperature is usually high, between 1020F and 1040F
 Rashes occur after onset of fever
 Fever subsides after a couple of days
 Other symptoms include headache, muscle
 pain, nausea, vomiting, fatigue, mouth ulcers, conjunctivitis, loss of taste, loss of appetite, etc. last for about 5
to 7 days.
 The severe muscle and joints pain makes
 movement difficult and prostates the person

Continue….
Chronic Phase
 Continued multiple joints pain that may persist from weeks to years
 95% of adults remain symptomatic for weeks to months with loss of mobility, decreased fine movements
of fingers, and slow reactions.
 Recurrent joints pain is seen in 30-40% victims
 Rarely, infections of heart muscle, brain coverings and bleeding have been recorded
 Death is rare and usually occurs in people over 65 or small children, especially those with other underlying

What causes chikungunya and how is it
transmitted?
 Over viewIt is a mosquito borne viral disease caused by
Chikungunya virus .
 The mosquitoes breed on stagnant water.
 The mosquitoes bite during daytime with peaks in early morning
and late afternoon
 Mosquitoes acquirethe virusfrom humans, and after a period of 8 to
10 days they transferit to other humans while feeding
 The viruscirculates in bloodof infected person for several days at
approximately the time when the person gets the fever

What are risk factors for chikungunya?
 Damp marshy areas.
 Areas with stagnant or collected water
 Mosquito prone areas
 Attendants of Chikungunya patients
 Individuals with weak immune systems
 Infection from mother to newborn
 during delivery
 Rainy season
 Old people or small children with other underlying illnesses

What can chikungunya lead to?
Most common complication is:
 Chronic Arthritis
Rare and serious complications are:
 Heart affections
 Inflammation of eye
 Acute kidney disease
 Inflammation of coverings of the brain
 Stroke and Paralysis
 Severe large skin lesions
 Infection from
 Rarely, death

Human Immune Response
 Flavivirus cause acute sporadic disease and are not persistent.
 The outcome of flavivirus infection in an animal is determined by a balance
between the speed of viral replication and spread, and the immune system
response.
 Flaviviruses have evolved specific tactics to evade the innate and adaptive immune
response.

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 Flaviviruses, have genomic size constraints, and are unable to acquire exogenous
genes.
 Smaller viruses evolve multifunctional genes that regulate viral life cycle, yet also
modulate the host response.
 The infected cells migrate to draining lymph nodes where arise early immune
response.
 Then reach secondary lymphoid tissues, leading to entry into the circulation via the
efferent lymphatic system and thoracic duct.

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 Now spread to visceral organs , then to neurotropic flaviviruses disseminate to the central nervous
system
 The mechanism by which flaviviruses avoid being targeted by its entry into brain and spinal cord remains
unclear
 There is an assumption that the virus enters via a haematogenous route.
 Flaviviruses may cross the blood–brain barrier by passive transport across the endothelium, by active
replication in endothelial cells.
 Trojan horse' mechanism in which the virus is carried into the brain by infected inflammatory cells
 The IFN-dependent innate immune response is essential for protection against flavivirus infections.
 Type I and II IFN inhibit flavivirus infection in cell culture and in animals.

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 Type I IFN block flavivirus infection by preventing translation and replication of
infectious viral RNA.
 Type II IFN inhibit flavivirus replication via the generation of proinflammatory and
antiviral molecules including nitric oxide .

DIAGNOSIS
 Can be confirmed by presence Zika virus RNA in the blood or other body fluids,
such as urine or saliva
 Zika virus RNA has been detected in urine up to 10 days after onset of the disease.
 From day five post onset of disease, serological investigations can be conducted by
detection of Zika-specific IgM antibodies and confirmation by neutralisation,
seroconversion or four-fold antibody titer increase of Zika specific antibodies in
paired serum samples.

AVAILABLE TREATMENT
 There is no vaccine or specific prophylactic treatment.
 Bharat biotech international company of India declared that they patented for
medicine for ZIKV.
 The treatment is symptomatic and mainly based on pain relief, fever reduction and
anti-histamines for pruritic rash.

PREVENTION
 The best form of prevention is protection against mosquito bites.
 Repellents should contain DEET (N, N-diethyl-3- methylbenzamide), IR3535 (3-[N-
acetyl-N-butyl]- aminopropionic acid ethyl ester) or icaridin (1 piperidinecarboxylic
acid, 2-(2-hydroxyethyl)-1- methylpropylester).

Chikungunya virus

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