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MARYAM JAMILAH BINTI ABDUL HAMID
082013100002
IMS BANGALORE
 Definition of viral haemorrhagic fever
 Exanthematous fever
 Mosquito borne diseases
A general term for a severe illness, sometimes
associated with bleeding, that may be caused by a
number of viruses (WHO)
Arbovirus
Arenavirus
Filovirus
Herpes
virus
ParamyxovirusPoxvirus
Togaviridae
Rhabdoviridae
Reoviridae
Bunyaviridae
Flaviviridae
1) ARBOVIRUS
o Togaviridae
Alfavirus
Rubivirus
o Flaviviridae
Mosquito borne diseases
Tick born fevers
o Bunyaviridae
Hantavirus
o Reoviridae
o Rhabdoviridae
2) POXVIRUS
o Small pox (variola)
3) HERPES VIRUS
o Chicken pox (HHV-3)
4) PARAMYXOVIRUS
o Measles (Measles virus)
5) FILOVIRUS
o Marburg virus
o Ebola virus
6) ARENAVIRUSES
o Lassa fever
o South America haemorrhagic
fever
 fever with skin eruption
POXVIRUS
 Small pox (variola)
HERPES VIRUS
 Chicken pox (HHV-3)
PARAMYXOVIRUS
 Measles (Measles virus)
Family: Poxviridae
Subfamily: Chordopoxvirinae
Genus: Orthopoxvirus
Virus: Variola
Morphology
 Enveloped DNA virus, Largest animal virus
(300x200x100 nm)
 Brick shaped
 Complex virus
 Nucleocapsids not symmetry
 V.S: biconcave double stranded DNA core surrounded
by double layered membrane
Viral Haemorrhagic Fevers
SMALL POX (Variola)
 Major scourge of humankind for at least 3000
years
 Global eradication in 1980
Pathogenesis
 Causative virus: poxvirus, IP: 7-17 days
 Host: human
 Forms: florid (fatal) in India –variola major
alastrim (non-fatal) in Latin America
–variola minor
 Mode of transmission:
◦ Contact by skin lesion
◦ Respiratory tract
Clinical Manifestation
 Fever
 Overall discomfort
 Headache
 Severe fatigue
 Severe back pain
 Vomiting
 Centrifugal vesicles
Viral Haemorrhagic Fevers
Viral Haemorrhagic Fevers
Lab diagnosis
 Light microscope
- Inclusion bodies:
Guarnieri bodies
 Culture
- CAM in chick embryo
- Tissue culture
(monkey kidney,
HeLa, chick embryo
cells)
- CPE >48 hr
- Rounding up of
individual cells
Prophylaxis
Prophylaxis
Vaccinia virus is used for small pox vaccination
-artificial virus, similar properties with variola virus
-broad host range; rabbit & mice
-may evolved from cowpox or smallpox
-cause localised skin infection
-vector for development of recombinant vaccines
Viral Haemorrhagic Fevers
Eradication is achieved because:-
 No subclinical infection or carrier state
 An effective vaccine
 No animal reservoir
 Aggressive surveillance-containment measure
 The only lab which stores variola virus
WHO Collaboration Centre, Atlanta, USA
Koltsovo, Russian Federation
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Virus: Varicella-zoster virus (DNA virus)
Life long latent infections
Morphology
 100-200 nm diameter
 Icosahedral capsid (162 capsomers)
 Linear double strand DNA
 Lipid envelope containing peplomers
 Tegument (between capsid & envelope)
 Multiply in the nuclei of infected cells
 Intranuclear inclusion bodies: Cowdry Type A
& peplomers
CHICKEN POX (Varicella-zoster virus)
 Commonest childhood exanthemata
 Primary infection in non-immune individual when
immunity falls to ineffective level
 Mode of transmission:
◦ Direct contact on skin lesion
◦ Inhalation by droplets from respiratory secretion & saliva
Pathogenesis
 Virus passes across surface epithelium in the
respiratory tract (no symptoms & detectable
lesion)
 IP: 7-23 days
 May cross placenta and causing viraemia in
pregnant woman
 May infect the foetus  congenital malformation
Clinical Manifestation
 Vesicular rash on the trunk
 Progress through macule, papule, vesicle, pustule
and scab
 Centripetal distribution
 Low grade fever
 Pruritis at the side of exanthemata
 More intense in adult
Complication
 Varicella pneumonia (common)
 Viral encephalitis & haemorrhagic varicella (rare)
Viral Haemorrhagic Fevers
Lab diagnosis:-
Direct
 Microscopy
◦ Tzanck smear
◦ Cowdry Type A intranuclear
inclusion bodies
 Culture
◦ Human fibroblast
◦ HeLa cells
◦ Human amnion
◦ CPE: syncytium formation slower than in HSV
 Direct fluorescent antibody
Indirect
 Specific antisera
(distinguish from HSV-1 & HSV-2)
Treatment
 Acyclovir
Prophylaxis
 Varicella vaccine from Oka strain
Viral Haemorrhagic Fevers
Viral Haemorrhagic Fevers
Family: Paramyxovirus
Genus: Morbillivirus
Virus: Measles virus
Origin: Human
Morphology
 Spherical enveloped
 120-250 nm diameter
 Envelope consists of lipoprotein membrane &
covered by projections
 Peplomers:
◦ H (haemagglutinin)
◦ F (fusion protein)
 Inner surface of the envelope covered by matrix
(M) protein
 Tightly coiled helical nucleocapsid
 Contains a single stranded negative sense RNA
genome and RNA-dependent RNA polymerase
Viral Haemorrhagic Fevers
MEASLES
 Highly infectious childhood disease
 Self limiting
 Once infected, life long immunity
Pathogenesis
 Mode of transmission: respiratory secretions
 IP: 10-12 days
Inhalation of measles virus
Epithelial surface (skin, mouth, respiratory tract, conjunctiva)
Secondary viraemia
Reticuloendothelial system & multiply
Invades bloodstream (primary viraemia)
Virus multiples in lymphoid tissue of respiratory track
Koplik’s spots (buccal mucosa),
widespread maculopapular rash (1st
at neck) –hypersensitivity type IV to
viral antigens
Rashes fade (a week)
Recover by 10-14 days
Viral Haemorrhagic Fevers
Viral Haemorrhagic Fevers
Viral Haemorrhagic Fevers
Viral Haemorrhagic Fevers
Complication
 Otitis media
 Bronchopneumonia
 Croup
 Giant cell pneumonia
 Post-measles encephalitis
 Subacute sclerosing panencephalitis (SSPE)
Lab diagnosis
 Most cases clinically diagnose but differential diagnosis need
lab study
 Samples collection: nasal secretion, throat washing, blood,
nasopharyngeal swab, conjunctiva
Direct
Microscopy
 Multinucleated giant cells from nasal secretion (Giemsa
stained) –even before rash appears
 Warthin finkeldey bodies; Intranuclear & intracytoplasmic
inclusion bodies (7-10 days)
Immunofluorescene; virus particle in exfoliated respiratory cells –
nasal secretion
Viral Haemorrhagic Fevers
Isolation
 Virus can be isolate after 2 days appearance of rash
 Virus can be obtained from urine after few more days
 Cultured in primary human embryo kidney, monkey
kidney or human amnion cells
 CPE: Intranuclear & intracytoplasmic inclusion bodies
(7-10 days)
 Immunofluorescene staining: monoclonal antibodies
Serology
 Serum is collected
 ELISA: Measles specific Ig M antibody
Confirmatory test (1-2 weeks after onset of rash)
 Haemagglutination inhibition (HI)
 Complement fixation test (CFT)
 Neutralisation tests on acute & convalescent sera
-4 fold rise in titre
 High titre measles antibody in CSF  SSPE
Epidemiology
 Natural host is man
 Monkeys acquire infection from man
 Maximum incidence in 1-5 y/o child
 Patients are infective 3 days before symptoms
manifest and till rash desquamates
 Virus enter through respiratory tract & conjunctiva
 Endemic throughout the world
 Epidemics in later winter and early spring
Prophylaxis
Active immunisation
 Edmonston strain
-live attenuated vaccine at age 9 months old
-passage through human kidney,amnion cell
cultures, chick embryo culture
-cause febrile rash
 Schwartz & Moraten strain
-safe but effective only in children15 months old
 Edmonston-Zagreb strain
-passage in human diploid cells
-produce seroconversion even in infant 4-6 months
-one dose by subcutaneous
 MMR vaccine (Measles, Mumps, Rubella)
-administered in 12 to 15 months old child
-subcutaneous injection
-lasting >20 years
-However, may not induce adequated antibody
response in young babies who possess maternal
antibodies
 Sabin
-live attenuated vaccine
-by intranasal aerosal
-induces good antibody response irrespective of the
presence of maternal antibodies
Passive immunisation
 Pooled sera containing antibody against
measles virus
 To: children with immunodeficiency, pregnant
women
ARBOVIRUS
Togaviridae (alphavirus)
 Chikungunya
Flaviviridae (flavivirus)
 Dengue
 Yellow fever
Family: Togaviridae
Genus: Alphavirus
Virus: Chikungunya virus
Africa, Europe, Asia, India and Pacific Oceans
Once infected, he or she is likely to be protected from
future infections
Morphology
 Enveloped RNA virus
 60-70 nm in diameter
 Icosahedral capsid
 Single strand positive sense RNA
Pathogenesis
 Vector: Aedes aegypti & Aedes albopictus
 Primary host: human
1. Bite of blood sucking mosquitoes
2. Virus multiplies in local lymph nodes
3. Variemia
4. May involve target organs leading to rash, arthritis,
hepatitis, nephritis and encephalitis
5. Capillary endothelium is involved
Clinical Manifestation
(3-7 days after bitten by infected mosquito)
 Fever
 Crippling joint pains (doubled-up)
 Lymphadenopathy
 Conjunctivitis
 Rash
Lab diagnosis
Sample collection
 Blood
Virus isolation
 Tissue culture
• Vero, BHK-21 & mosquito cell lines
• Growth identified by immunofluorescence,
haemagglutination inhibition, complement fixation,
ELISA or neutralisation
 Insect vectors & reservoir animal
Serology
 ELISA
-serotype specific IgM antibody (within 1-3 days
after onset of illness)
-4 fold rise or more in antibody titre
 CFT
 Haemagglutination inhibition test or neutralisation
test
Treatment
 There is no medicine to treat chikungunya virus
infection or disease.
 Decrease the symptoms:
◦ Get plenty of rest
◦ Drink fluids to prevent dehydration
◦ Take medicines, such as ibuprofen, naproxen,
acetaminophen, or paracetamol, to relieve fever and
pain.
Prophylaxis
 No vaccine exists to prevent chikungunya virus
infection or disease
 Prevent chikungunya virus infection by avoiding
mosquito bites
 The mosquitoes that spread the chikungunya virus
bite mostly during the daytime
Viral Haemorrhagic Fevers
Family: Flaviviridae
Genus: Flavivirus
Virus: Yellow fever virus
 ‘Yellow quarantine flag’
 Tropical and subtropical areas in South America
and Africa
 Illness ranges in severity from a self-limited febrile
illness to severe liver disease with bleeding
Morphology
 Envelope RNA virus
 Spherical 40-50 nm in
diameter
 Single stranded positive
sense RNA
 Inner viral core surrounded
by lipid envelope which is
covered with glycoprotein
peplomers & matrix or
membrane protein
Pathogenesis (IP: 3-6 days)
 2 forms it can occurs; urban cycle & forest or
sylvatic cycle
 Urban cycle
Reservoir & definitive host :Man
Vector: Aedes aegypti mosquito
 Forest or sylvatic cycle
Reservoir: wild monkeys
Vectors: forest mosquitoes
Aedes africanus (Africa)
Haemagogus spegazzinii (S.America)
-Human infected when trespass into the forest or
when monkeys raid villages
Clinical Manifestation
 Fever with chills
 Headache
 Myalgia
 Vomiting
 Severe jaundice (extensive destruction of liver)
 Death 20-50% in severe cases
Lab diagnosis
Sample collection
 Blood, liver biopsy
Virus isolation
 Tissue culture
• Vero, BHK-21 & mosquito cell lines
• Growth identified by immunofluorescence,
haemagglutination inhibition, complement fixation,
ELISA or neutralisation
 Insect vectors & reservoir animal
Serology
 ELISA
-serotype specific IgM antibody (within 1-3 days
after onset of illness)
-4 fold rise or more in antibody titre
 CFT
 Haemagglutination inhibition test or neutralisation
test
Treatment
 There is no specific treatment for yellow fever
Prophylaxis
 17 D vaccine
 French neurotropic vaccine (Dakar)
 Steps to prevent yellow fever virus infection
include using insect repellent, wearing protective
clothing, and getting vaccinated
Family: Flaviviridae
Genus: Flavivirus
Virus: Dengue virus
Also known as ‘break-bone fever’
Asia, the Caribbean, the Pacific, West Africa, India
(East coast)
Morphology
Similar to yellow fever
Pathogenesis
 4 serotypes; DEN 1, DEN 2, DEN 3, DEN 4
 Vector: Aedes aegypti
1) Classical dengue fever
2) Dengue haemorrhagic fever
3) Dengue shock syndrome
 Usually affects older children & adults
 Bite from the infected mosquito enters the blood
stream
 Biphasic fever (saddle back), headache, pain in
muscles & bones
 IP: 5-8 days
 Maculopapular rash appears on 3rd or 4th day
 Febrile illness lasts for about 10 days
 Complete recovery and rarely fatal
 More serious form; Hyperimmune response
 Mostly confined among children 5-10 y/o in area
where multiple dengue viruses cause disease
 Seen in patients previously infected with dengue
virus
 On reinfection with a different serotype, antibody
formed against the first virus reacts with the
second serotype virus forming immune complexes
(virus-antibody complex)
 Symptoms like those of dengue fever but
associated with haemorrhagic rash,
thrombocytopenia & shock
Clinical Manifestation
 Fever of sudden onset
 Headache
 Retrobulbar pain
 Conjunctival infection
 Pain in the back & joints
 Lymphadenopathy
 Maculopapular rash
Lab diagnosis
Specimens
 Antibody & antigen detection: serum
 Isolation of virus and PCR: serum, plasma, whole
blood (washed buffy coat), autopsy tissue,
mosquitoes collected in nature
Haematological diagnosis
 Thrombocytopenia (1 lakh or less per mm3)
 Haemoconcentration (>20% rise in haematocrit)
Microbiological diagnosis
Serology plays important role
Detect antibody
 ELISA
–Ig M (5 days after onset & persist 1-3 months)
–Ig G (later than Ig M), 4 folds rise titre in paired
sera taken at an interval of 10 days *confirmatory
 Strip of immunochromatographic test (rapid test)
–Ig M
Detection of NS1 antigen
 Immunochromatographic test (Rapid test)
1st day of fever before antibodies appear
It takes 15 minutes
Isolation of virus
 Inoculate virus into mosquitoes, mosquitoes cell
lines (C6/36 or AP-61 cells), or suckling mice
 Further identification by fluorescent antibody test
Polymerase Chain Reaction (PCR)
 Viral RNA can be detected in clinical specimens by
reverse transcriptase polymerase chain reaction
(RTPCR)
 Viral genomic can be detected
Treatment
 Symptomatic treatment
 If severe, infuse platelets to reduce the haemorrhagic
manifestation
Prophylaxis
 No effective vaccine available
 Elimination of the mosquitoes (Aedes aegypti)
 To avoid DHF/DSS in immunised persons, a live
attenuated vaccine containing all serotypes
(clinical trials)
Topics covered are:
 Exanthematous fever
◦ Smallpox, chickenpox, measles
 Mosquito borne diseases
◦ Chikungunya, yellow fever, dengue
 Mim’s Medical Microbiology, 5th edition
 Textbook of Microbiology, Baveja, 4th edition
 Internet
 www.cdc.gov
Viral Haemorrhagic Fevers

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Viral Haemorrhagic Fevers

  • 1. MARYAM JAMILAH BINTI ABDUL HAMID 082013100002 IMS BANGALORE
  • 2.  Definition of viral haemorrhagic fever  Exanthematous fever  Mosquito borne diseases
  • 3. A general term for a severe illness, sometimes associated with bleeding, that may be caused by a number of viruses (WHO)
  • 5. 1) ARBOVIRUS o Togaviridae Alfavirus Rubivirus o Flaviviridae Mosquito borne diseases Tick born fevers o Bunyaviridae Hantavirus o Reoviridae o Rhabdoviridae 2) POXVIRUS o Small pox (variola) 3) HERPES VIRUS o Chicken pox (HHV-3) 4) PARAMYXOVIRUS o Measles (Measles virus) 5) FILOVIRUS o Marburg virus o Ebola virus 6) ARENAVIRUSES o Lassa fever o South America haemorrhagic fever
  • 6.  fever with skin eruption POXVIRUS  Small pox (variola) HERPES VIRUS  Chicken pox (HHV-3) PARAMYXOVIRUS  Measles (Measles virus)
  • 7. Family: Poxviridae Subfamily: Chordopoxvirinae Genus: Orthopoxvirus Virus: Variola Morphology  Enveloped DNA virus, Largest animal virus (300x200x100 nm)  Brick shaped  Complex virus  Nucleocapsids not symmetry  V.S: biconcave double stranded DNA core surrounded by double layered membrane
  • 9. SMALL POX (Variola)  Major scourge of humankind for at least 3000 years  Global eradication in 1980 Pathogenesis  Causative virus: poxvirus, IP: 7-17 days  Host: human  Forms: florid (fatal) in India –variola major alastrim (non-fatal) in Latin America –variola minor  Mode of transmission: ◦ Contact by skin lesion ◦ Respiratory tract
  • 10. Clinical Manifestation  Fever  Overall discomfort  Headache  Severe fatigue  Severe back pain  Vomiting  Centrifugal vesicles
  • 13. Lab diagnosis  Light microscope - Inclusion bodies: Guarnieri bodies  Culture - CAM in chick embryo - Tissue culture (monkey kidney, HeLa, chick embryo cells) - CPE >48 hr - Rounding up of individual cells
  • 15. Prophylaxis Vaccinia virus is used for small pox vaccination -artificial virus, similar properties with variola virus -broad host range; rabbit & mice -may evolved from cowpox or smallpox -cause localised skin infection -vector for development of recombinant vaccines
  • 17. Eradication is achieved because:-  No subclinical infection or carrier state  An effective vaccine  No animal reservoir  Aggressive surveillance-containment measure  The only lab which stores variola virus WHO Collaboration Centre, Atlanta, USA Koltsovo, Russian Federation
  • 18. Family: Herpesviridae Subfamily: Alphaherpesvirinae Virus: Varicella-zoster virus (DNA virus) Life long latent infections Morphology  100-200 nm diameter  Icosahedral capsid (162 capsomers)  Linear double strand DNA  Lipid envelope containing peplomers  Tegument (between capsid & envelope)  Multiply in the nuclei of infected cells  Intranuclear inclusion bodies: Cowdry Type A
  • 20. CHICKEN POX (Varicella-zoster virus)  Commonest childhood exanthemata  Primary infection in non-immune individual when immunity falls to ineffective level  Mode of transmission: ◦ Direct contact on skin lesion ◦ Inhalation by droplets from respiratory secretion & saliva
  • 21. Pathogenesis  Virus passes across surface epithelium in the respiratory tract (no symptoms & detectable lesion)  IP: 7-23 days  May cross placenta and causing viraemia in pregnant woman  May infect the foetus  congenital malformation
  • 22. Clinical Manifestation  Vesicular rash on the trunk  Progress through macule, papule, vesicle, pustule and scab  Centripetal distribution  Low grade fever  Pruritis at the side of exanthemata  More intense in adult Complication  Varicella pneumonia (common)  Viral encephalitis & haemorrhagic varicella (rare)
  • 24. Lab diagnosis:- Direct  Microscopy ◦ Tzanck smear ◦ Cowdry Type A intranuclear inclusion bodies  Culture ◦ Human fibroblast ◦ HeLa cells ◦ Human amnion ◦ CPE: syncytium formation slower than in HSV  Direct fluorescent antibody
  • 25. Indirect  Specific antisera (distinguish from HSV-1 & HSV-2) Treatment  Acyclovir Prophylaxis  Varicella vaccine from Oka strain
  • 29. Morphology  Spherical enveloped  120-250 nm diameter  Envelope consists of lipoprotein membrane & covered by projections  Peplomers: ◦ H (haemagglutinin) ◦ F (fusion protein)  Inner surface of the envelope covered by matrix (M) protein  Tightly coiled helical nucleocapsid  Contains a single stranded negative sense RNA genome and RNA-dependent RNA polymerase
  • 31. MEASLES  Highly infectious childhood disease  Self limiting  Once infected, life long immunity Pathogenesis  Mode of transmission: respiratory secretions  IP: 10-12 days
  • 32. Inhalation of measles virus Epithelial surface (skin, mouth, respiratory tract, conjunctiva) Secondary viraemia Reticuloendothelial system & multiply Invades bloodstream (primary viraemia) Virus multiples in lymphoid tissue of respiratory track Koplik’s spots (buccal mucosa), widespread maculopapular rash (1st at neck) –hypersensitivity type IV to viral antigens Rashes fade (a week) Recover by 10-14 days
  • 37. Complication  Otitis media  Bronchopneumonia  Croup  Giant cell pneumonia  Post-measles encephalitis  Subacute sclerosing panencephalitis (SSPE)
  • 38. Lab diagnosis  Most cases clinically diagnose but differential diagnosis need lab study  Samples collection: nasal secretion, throat washing, blood, nasopharyngeal swab, conjunctiva Direct Microscopy  Multinucleated giant cells from nasal secretion (Giemsa stained) –even before rash appears  Warthin finkeldey bodies; Intranuclear & intracytoplasmic inclusion bodies (7-10 days) Immunofluorescene; virus particle in exfoliated respiratory cells – nasal secretion
  • 40. Isolation  Virus can be isolate after 2 days appearance of rash  Virus can be obtained from urine after few more days  Cultured in primary human embryo kidney, monkey kidney or human amnion cells  CPE: Intranuclear & intracytoplasmic inclusion bodies (7-10 days)  Immunofluorescene staining: monoclonal antibodies
  • 41. Serology  Serum is collected  ELISA: Measles specific Ig M antibody Confirmatory test (1-2 weeks after onset of rash)  Haemagglutination inhibition (HI)  Complement fixation test (CFT)  Neutralisation tests on acute & convalescent sera -4 fold rise in titre  High titre measles antibody in CSF  SSPE
  • 42. Epidemiology  Natural host is man  Monkeys acquire infection from man  Maximum incidence in 1-5 y/o child  Patients are infective 3 days before symptoms manifest and till rash desquamates  Virus enter through respiratory tract & conjunctiva  Endemic throughout the world  Epidemics in later winter and early spring
  • 43. Prophylaxis Active immunisation  Edmonston strain -live attenuated vaccine at age 9 months old -passage through human kidney,amnion cell cultures, chick embryo culture -cause febrile rash  Schwartz & Moraten strain -safe but effective only in children15 months old  Edmonston-Zagreb strain -passage in human diploid cells -produce seroconversion even in infant 4-6 months -one dose by subcutaneous
  • 44.  MMR vaccine (Measles, Mumps, Rubella) -administered in 12 to 15 months old child -subcutaneous injection -lasting >20 years -However, may not induce adequated antibody response in young babies who possess maternal antibodies  Sabin -live attenuated vaccine -by intranasal aerosal -induces good antibody response irrespective of the presence of maternal antibodies
  • 45. Passive immunisation  Pooled sera containing antibody against measles virus  To: children with immunodeficiency, pregnant women
  • 46. ARBOVIRUS Togaviridae (alphavirus)  Chikungunya Flaviviridae (flavivirus)  Dengue  Yellow fever
  • 47. Family: Togaviridae Genus: Alphavirus Virus: Chikungunya virus Africa, Europe, Asia, India and Pacific Oceans Once infected, he or she is likely to be protected from future infections Morphology  Enveloped RNA virus  60-70 nm in diameter  Icosahedral capsid  Single strand positive sense RNA
  • 48. Pathogenesis  Vector: Aedes aegypti & Aedes albopictus  Primary host: human 1. Bite of blood sucking mosquitoes 2. Virus multiplies in local lymph nodes 3. Variemia 4. May involve target organs leading to rash, arthritis, hepatitis, nephritis and encephalitis 5. Capillary endothelium is involved
  • 49. Clinical Manifestation (3-7 days after bitten by infected mosquito)  Fever  Crippling joint pains (doubled-up)  Lymphadenopathy  Conjunctivitis  Rash
  • 50. Lab diagnosis Sample collection  Blood Virus isolation  Tissue culture • Vero, BHK-21 & mosquito cell lines • Growth identified by immunofluorescence, haemagglutination inhibition, complement fixation, ELISA or neutralisation  Insect vectors & reservoir animal
  • 51. Serology  ELISA -serotype specific IgM antibody (within 1-3 days after onset of illness) -4 fold rise or more in antibody titre  CFT  Haemagglutination inhibition test or neutralisation test
  • 52. Treatment  There is no medicine to treat chikungunya virus infection or disease.  Decrease the symptoms: ◦ Get plenty of rest ◦ Drink fluids to prevent dehydration ◦ Take medicines, such as ibuprofen, naproxen, acetaminophen, or paracetamol, to relieve fever and pain.
  • 53. Prophylaxis  No vaccine exists to prevent chikungunya virus infection or disease  Prevent chikungunya virus infection by avoiding mosquito bites  The mosquitoes that spread the chikungunya virus bite mostly during the daytime
  • 55. Family: Flaviviridae Genus: Flavivirus Virus: Yellow fever virus  ‘Yellow quarantine flag’  Tropical and subtropical areas in South America and Africa  Illness ranges in severity from a self-limited febrile illness to severe liver disease with bleeding
  • 56. Morphology  Envelope RNA virus  Spherical 40-50 nm in diameter  Single stranded positive sense RNA  Inner viral core surrounded by lipid envelope which is covered with glycoprotein peplomers & matrix or membrane protein
  • 57. Pathogenesis (IP: 3-6 days)  2 forms it can occurs; urban cycle & forest or sylvatic cycle  Urban cycle Reservoir & definitive host :Man Vector: Aedes aegypti mosquito  Forest or sylvatic cycle Reservoir: wild monkeys Vectors: forest mosquitoes Aedes africanus (Africa) Haemagogus spegazzinii (S.America) -Human infected when trespass into the forest or when monkeys raid villages
  • 58. Clinical Manifestation  Fever with chills  Headache  Myalgia  Vomiting  Severe jaundice (extensive destruction of liver)  Death 20-50% in severe cases
  • 59. Lab diagnosis Sample collection  Blood, liver biopsy Virus isolation  Tissue culture • Vero, BHK-21 & mosquito cell lines • Growth identified by immunofluorescence, haemagglutination inhibition, complement fixation, ELISA or neutralisation  Insect vectors & reservoir animal
  • 60. Serology  ELISA -serotype specific IgM antibody (within 1-3 days after onset of illness) -4 fold rise or more in antibody titre  CFT  Haemagglutination inhibition test or neutralisation test
  • 61. Treatment  There is no specific treatment for yellow fever Prophylaxis  17 D vaccine  French neurotropic vaccine (Dakar)  Steps to prevent yellow fever virus infection include using insect repellent, wearing protective clothing, and getting vaccinated
  • 62. Family: Flaviviridae Genus: Flavivirus Virus: Dengue virus Also known as ‘break-bone fever’ Asia, the Caribbean, the Pacific, West Africa, India (East coast) Morphology Similar to yellow fever
  • 63. Pathogenesis  4 serotypes; DEN 1, DEN 2, DEN 3, DEN 4  Vector: Aedes aegypti 1) Classical dengue fever 2) Dengue haemorrhagic fever 3) Dengue shock syndrome
  • 64.  Usually affects older children & adults  Bite from the infected mosquito enters the blood stream  Biphasic fever (saddle back), headache, pain in muscles & bones  IP: 5-8 days  Maculopapular rash appears on 3rd or 4th day  Febrile illness lasts for about 10 days  Complete recovery and rarely fatal
  • 65.  More serious form; Hyperimmune response  Mostly confined among children 5-10 y/o in area where multiple dengue viruses cause disease  Seen in patients previously infected with dengue virus
  • 66.  On reinfection with a different serotype, antibody formed against the first virus reacts with the second serotype virus forming immune complexes (virus-antibody complex)  Symptoms like those of dengue fever but associated with haemorrhagic rash, thrombocytopenia & shock
  • 67. Clinical Manifestation  Fever of sudden onset  Headache  Retrobulbar pain  Conjunctival infection  Pain in the back & joints  Lymphadenopathy  Maculopapular rash
  • 68. Lab diagnosis Specimens  Antibody & antigen detection: serum  Isolation of virus and PCR: serum, plasma, whole blood (washed buffy coat), autopsy tissue, mosquitoes collected in nature Haematological diagnosis  Thrombocytopenia (1 lakh or less per mm3)  Haemoconcentration (>20% rise in haematocrit)
  • 69. Microbiological diagnosis Serology plays important role Detect antibody  ELISA –Ig M (5 days after onset & persist 1-3 months) –Ig G (later than Ig M), 4 folds rise titre in paired sera taken at an interval of 10 days *confirmatory  Strip of immunochromatographic test (rapid test) –Ig M
  • 70. Detection of NS1 antigen  Immunochromatographic test (Rapid test) 1st day of fever before antibodies appear It takes 15 minutes Isolation of virus  Inoculate virus into mosquitoes, mosquitoes cell lines (C6/36 or AP-61 cells), or suckling mice  Further identification by fluorescent antibody test
  • 71. Polymerase Chain Reaction (PCR)  Viral RNA can be detected in clinical specimens by reverse transcriptase polymerase chain reaction (RTPCR)  Viral genomic can be detected Treatment  Symptomatic treatment  If severe, infuse platelets to reduce the haemorrhagic manifestation
  • 72. Prophylaxis  No effective vaccine available  Elimination of the mosquitoes (Aedes aegypti)  To avoid DHF/DSS in immunised persons, a live attenuated vaccine containing all serotypes (clinical trials)
  • 73. Topics covered are:  Exanthematous fever ◦ Smallpox, chickenpox, measles  Mosquito borne diseases ◦ Chikungunya, yellow fever, dengue
  • 74.  Mim’s Medical Microbiology, 5th edition  Textbook of Microbiology, Baveja, 4th edition  Internet  www.cdc.gov

Editor's Notes

  1. Scourge= causing death
  2. Small,shiny,white,convex,non-necrotic,non-haemorrhagic, Guarnieri bodies (intracytoplasmic inclusion bodies). Inclusion bodies= virus-specific intracellular globular masses which are produced during replication of virus in host cells
  3. Tzank smear Unroof vesicle and scrape base w/ sterile surgical blade Smear onto clean glass slide Fix w/ gentle heat or air dry Fix w/ MeOH (methanol) Stain w/ Giemsa, methylene blue or Wright’s stain Microscopic examination using oil immersion lens. (Look for multinucleate giant cells)
  4. Croup is breathing difficulty and a "barking" cough. Croup is due to swelling around the vocal cords. It is common in infants and children. SSPE is also known as Dawson Disease, Dawson encephalitis and measles encephalitis. It should not be confused with acute disseminated encephalomyelitis which has a similar etiology but very different timing and course. Subacute sclerosing panencephalitis (SSPE) is a rare chronic, progressive encephalitis that affects primarily children and young adults, caused by a persistent infection with measles virus (which can be a result of a mutation of the virus itself). It has been estimated that about 1 in 10,000 people infected with measles will eventually develop SSPE.[1] No cure for SSPE exists and the condition often ends fatally, but it can be managed by medication if treatment is started at an early stage. Much of the work on SSPE has been performed by the National Institute of Neurological Disorders and Stroke (NINDS).
  5. Baby Hamster Kidney Fibroblast Cells (BHK-21 Line)
  6. Baby Hamster Kidney Fibroblast Cells (BHK-21 Line)