Chikungunya- a short PPT. This tells in brief about the infection. The neurological complications is the main focus. The management and other related issues are also discussed.

1. CHIKUNGUNYA

2. INTRODUCTION
• Chikungunya virus (CHIKV) is an insect-borne virus
• Genus- Alphavirus
• Family- Togaviridae
• VECTOR- AEDES MOSQUITO(AEDES AEGYPTI, AEDES ALBOPICTUS)
• FIRST RECOGNIZED IN EPIDEMIC FORM IN EAST AFRICA IN 1952-
1953.
• In India CHIKV was first isolated in CALCUTTA in 1963, with several
reported outbreaks in India since then.

3. INTRODUCTION
• The name ‘Chikungunya’ is derived from the Makonde word
meanings “that which bends up” in reference to the stooped
posture which develops as a result of arthritic symptoms of
the disease.

4. INTRODUCTION
• The disease was first described by Marion Robinson and
W.H.R. Lumsden in 1955, following an outbreak on the
Makonde Plateau, along the border between Tanganyika and
Mozambique in 1952.
• It had caused two major outbreaks, one in Calcutta during
month of July-August 1963 and another in Madras and Vellore
cities of Chennai state during months of July–November 1964.

5. RECENT OUTBREAKS

7. PATHOGENESIS

11. CLINICAL FEATURES

12. FEVER AND CONSTITUTIONAL
SYMPTOMS
• the incubation period is typically 3–7 days(range, 1–12 days)
• fever - abrupt and associated with chills and joint pain.
• Fever was moderate (100-103 F) for first 7 days,
• There after, became mild (99-1000F) for next 3-4 days.
• Aassociated headache, myalgia, lethargy, insomnia and
anorexia with fever.

13. MUSCULOSKELETAL SYMPTOMS/SIGNS
 THE MOST STRIKING COMPLAINT WITH FEVER WAS JOINT PAIN
sudden in onset
moderate to severe in severity and
 had affected more than one joint at a time.
 The joints involved in order of severity and preference were knee,
ankle, wrist, small joints of hand & feet and elbow.
 Because of severe pains the most of the cases were confined to
bed on 1st or 2nd day of fever and developed characteristic
stooped flexed posture.

15. GIT SYMPTOMS/SIGNS
• Vomitings,
• Stomatitis
• Oral ulceration
• Mild hepatomegaly.

17. NEUROLOGICAL
COMPLICATIONS

18. NEUROLOGICAL COMPLICATIONS
• CHIKV infection first reported to affect the
nervous system in 1960s.
• Neurological complications have been
reported in various studies from 9% to 25%.
• Adults – 2nd to 3rd day
• Children- early within 24hrs after the onset of
fever

19. NEUROLOGICAL COMPLICATIONS
• Manifestations can be
 Early /acute phase
 Late - immune mediated

20. Early /acute phase
• ENCEPHALITIS
• MENINGOENCEPHALITIS
• SEIZURES
• CEREBELLAR SYNDROME
• MYELITIS
• MYELONEUROPATHY
• CRANIAL NEUROPATHIES - OPTIC NERVE,
OPHTHALMOPLEGIA, FACIAL NERVE AND SNHL
• STROKE
• NEUROPATHY

21. LATE PHASE - IMMUNE MEDIATED
• GBS
• OPTIC NEURITIS
• RETRO BULBAR NEURITIS
• MYELITIS

22. ENCEPHALOPATHY
• Encephalopathy is most commonly seen and
can be the isolated neurologic finding and the
most prominent feature
• It is observed in the first few days after fever
with headache, altered sensorium, with
seizures
• Transient focal signs were rare: ataxia , focal
rigidity and opsoclonus .

23. Myelopathy
• Myelopathy can be in isolation or along with encepalopathy
• It started a few days after fever.
• Patient often firrst developed retention of urine and then showed
paraparesis.
• Usually, the upper limbs were more or less not involved
• The CSF showed raised proteins and lymphocytic pleocytosis .
• The MRI rarely showed cord changes .

24. NEUROPATHY
• two types of neuropathy.
• Early neuropathy :
• These presented within few days of the onset of fever.
• These patients had additional encephalopathy or myelopathy
• In early neuropathy, the patient rapidly developed
quadriparesis and many of them had facial weakness and
required a ventilator.
• Late neuropathy : occurred and presented few weeks after
the onset of fever.
• These were oft en with a pure syndrome .

25. NEUROPATHY
• The NCV in these cases showed axonal sensory motor
neuropathy.
• The CSF shows raised proteins and lymphocytic pleocytosis.
• Cells varied from nil to 12/cmm
• Neuropathy often did not improve well with IVIg or
plasmapheresis

26. NEUROPATHY
• In this early neuropathy, the features that
were found to be different from typical
Guillain-Barre Syndrome were
• 1. Almost always axonal
• 2. CSF pleocytosis
• 3. Additional signs in many of myelopathy/
encephalopathy
• 4. Response to plasmapheresis/ IVIg
infrequent .

27. CARPAL TUNNEL SYNDROME
• It occurs rarely.
• It occurs several weeks after Chikungunya.
• In these cases, the wrist synovitis was ++ with severe pain in
hand that was considerably severe than usual, and pain was
bilateral.
• Median nerve territory weakness was noted .
• During early neuropathy, often noted that the median nerve
findings of motor amplitude and distal latency were
considerably worse than in the ulnar

28. CARPAL TUNNEL SYNDROME
• Apparently, carpal tunnel syndrome does not
imply entry of virus into the nervous system
and it was secondary to synovitis

29. ?The important question is whether the
neurologic manifestation is infectious or an
immune-mediated postinfectious
phenomenon

30. Likely to be infectious because of the
following reasons:
 Neurological features arise with febrile
illness
 Lesions on MRI are certainly not similar to
any cases of acute disseminated encephalitis
 IgM antibodies to Chikungunya in CSF.
 Pleocytosis in CSF.
 Virus isolation from CSF

31. Death in Chikungunya Neurology
• In one study 13.5% of patients with
neurological involvement .
• All had severe encephalopathy at onset.
• Additional features of myelopathy and
neuropathy were found
• All were >55 years of age.

32. LABORATORY DIAGNOSIS

33. LABORATORY DIAGNOSIS
• The clinical manifestations of Chikungunya fever resemble
those of dengue fever, laboratory diagnosis is critical to
establish the cause of disease
• Three main laboratory tests are used for diagnosing
Chikungunya fever:
 VIRUS ISOLATION,
 SEROLOGICAL TESTS AND
 MOLECULAR TECHNIQUE OF POLYMERASE CHAIN
REACTION (PCR).

36. CHIKUNGUNYA IGM CARD TEST
(CTK BIOTECH)
• It is the onsite Chikungunya IgM rapid test that is a lateral flow
chromatographic immuno-assay for the qualitative detection of IgM
anti Chikungunya virus “Chik–V” in the human serum or plasma.
• IT IS A SCREENING TEST
• The onsite Chikungunya IgM rapid card test is an IgM capture
immunoassay, utilizing recombinant antigen derived from its
structural protein.
• It detects IgM anti-chikungunya in patient’s serum or plasma within
10 minutes.

37. RT-PCR
• Recently, a REVERSE TRANSCRIPTASE, RT-PCR TECHNIQUE for
diagnosing CHIK virus has been developed using nested primer pairs
amplifying specific components of three structural gene regions,
 Capsid (C),
Envelope E-2 and
part of Envelope E1.
• PCR results can be available from within 1-2 days.
• Specimens for PCR is same as the virus isolation i.e. heparinized
whole blood.

38. VIRUS ISOLATION
• Virus isolation is the most definitive test.
• Between 2-5 ml of whole blood is collected during the first week of illness
in commercial heparinized tube and transported on ice to the laboratory.
• The CHIK virus produces cytopathic effects in a variety of cell lines
including BHK-21, HeLa and Vero cells.
• The cytopathic effects must be confirmed by CHIK specific antiserum and
the results can take between 1-2 weeks.
• Virus isolation must only be carried in BSL-3 laboratories to reduce the risk
of viral transmission.

40. A, Bilateral frontoparietal white matter lesions with restricted diffusion.
K. Ganesan et al. AJNR Am J Neuroradiol 2008;29:1636-
1637
©2008 by American Society of Neuroradiology

41. • Axial cranial magnetic
resonance imaging with
fluid-attenuated
inversion recovery of
showing confluent and
large multiple hyper
intense signals within
both periventricular
white matters.

42. Case Definition of CHK fever
• Suspect case:- acute onset, high fever,7days duration, severe
headache, myalgia, severe arthralgia,with or without rash
• Probable Case:-suspect case of CHK,high vector
dencity,presence of confirm case in the area .
• Confirmed Case:-
• Isolation of virus in early phase.
• Serological test for IgM antibody after 5th day of illness.
• Demonstration of 4 fold or greater rise in IgG antibodies in
paired sera.

43. • Self-limiting and Will Resolve With Time.
• NO SPECIFIC TREATMENT FOR CHIKUNGUNYA.
• Supportive or Palliative Medical Care With Anti-
inflammatories .
• Supportive care with rest is indicated during the
acute joint symptoms.
TREATMENT

44. TREATMENT
• Movement and mild exercise tend to improve
stiffness and morning arthralgia, but heavy
exercise may exacerbate rheumatic symptoms.
• Apirin and nonsteroidal antiinflammatory drugs,
chloroquine phosphate (250 mg/day) has given
promising results.

45. IMMUNOTHERAPY
• INDICATED in
 GBS
 OPTIC NEURITIS
 MYELITIS

46. OPTIC NEURITIS
• IV METHYL PREDNISOLONE 1000mg/day for 3
days , followed by oral PREDNISOLONE
tapperd over few weeks

47. PREVENTION
• Elimination of stagnant water at home, schools and
work place to avoid breeding of mosquitoes.
• Using insect repellents over the exposed parts of the
body.
• Using mosquito screens or nets in non – Air-
conditioned rooms.
• Wearing the long sleeved clothes like long trousers of
a light shade for protection against mosquitoes.

48. Is there any vaccine?
• Currently there is no marketable vaccine
available .
• Chikungunya confers a life-long immunity on
the infected person.

49. THANK YOU