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Arboviral disease and dengue
The document discusses various aspects of arboviruses, focusing primarily on dengue fever, including its epidemiology, pathogenesis, clinical features, diagnosis, and management strategies. It highlights the dengue virus as a major global health issue, endemic in over 100 countries, and outlines the role of mosquitoes as vectors in transmission. Additionally, the document addresses the challenges in developing dengue vaccines and provides insights into other arboviral diseases like chikungunya and zika.
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Dr. Tarek Mahbub Khan's focus on the epidemiology, types, pathogenesis, and treatment of dengue.
Arboviruses are zoonotic, arthropod-borne viruses. Transmission cycles include both vertical and horizontal methods.
Initial viral replication leads to various clinical syndromes including fever and encephalitis.
Key laboratory techniques include viral culture, PCR, and serology for diagnosis of arboviruses.
Dengue, caused by a single-stranded RNA virus, is endemic in over 100 countries with high incidence.
Key vectors include Aedes mosquitoes, with urban and jungle reservoirs for the dengue virus.
Classical dengue and dengue hemorrhagic fever are discussed, including their distinct pathological changes.
Clinical symptoms and phases of dengue, including critical signs of dengue hemorrhagic fever.
Overview of immune response, laboratory tests, and CBC findings for dengue diagnosis.
Symptomatic treatment and prevention methods, highlighting the absence of licensed dengue vaccines.
Overview of different proposed types of dengue vaccines under development.
Introduction to chikungunya virus, its transmission, reservoirs, and geographic distribution.
Symptoms include fever, joint pain, and a rash; hemorrhagic symptoms are rare.
Diagnosis based on travel history and clinical features; treatment is mainly symptomatic.
Zika virus shares properties with dengue and causes various symptoms; understanding incubation.
Common symptoms include fever and rash; vertical transmission can occur from mother to fetus.
Laboratory tests for Zika include PCR and serology; management focuses on symptomatic care.
Listed references for further reading on medical microbiology and epidemiology of arboviruses.
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Arboviral disease and dengue
- 1. Dr. Tarek MahbubKhan MBBS, M.Phil Assistant Professor Department of Virology 1Dr. Tarek/SSMC/2016
- 2. TLO • Epidemiology • Typesof dengue fever • Pathogenesis and pathology of dengue • Clinical features • Phases of dengue hemorrhagic fever• Phases of dengue hemorrhagic fever • Treatment and prevention of dengue • Latest advancement of dengue vaccine development 2Dr. Tarek/SSMC/2016
- 3. ARBOVIRUS • Arbovirus arearthropod-borne viruses • Human arboviruses all are believed to be zoonotic • Vectors acquire a lifelong infection • Natural cycle can be maintained by transovarian transmission in arthropods • Humans are the accidental host 2/1/2017 3Dr. Tarek/kuin/2015
- 4. CLASSIFICATION OF MAJOR ARBOVIRUSES FamilyGenus Virus of medical importance Togaviridae Alphavirus Chikungunya, EEE, WEE, VEE, Sinbis viruses Flaviviridae Flavivirus Dengue, JEV, YFV, WNV,Flaviviridae Flavivirus Dengue, JEV, YFV, WNV, St. Louis encephalitis virus Bunyaviridae Bunyavirus Bunyamwera, La Crosse, California encephalitis virus Reoviridae Coltivirus Colorado tick fever virus 2/1/2017 4Dr. Tarek/kuin/2015
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- 6. CHARACTERISTICS OF LIFECYCLE • Virus has the ability to replicate in the vertebrate host as well as blood sucking vector • EXTRINSIC INCUBATION PERIOD: Time required for the virus to• EXTRINSIC INCUBATION PERIOD: Time required for the virus to form sufficient progeny in the vector. Usually 7-14 days • INTRINSIC INCUBATION PERIOD: Time interval between vector bite and appearance of symptom in human 2/1/2017 6Dr. Tarek/kuin/2015
- 7. • VERTICAL TRANSMISSION(TRANSOVARIAN): –From infected mother vector to her offspring. • HORIZONTAL TRANSMISSION: – From infected vector to human CHARACTERISTICS OF LIFE CYCLE – From infected vector to human • Human is the dead end host (except: YF and Dengue) 2/1/2017 Dr. Tarek/kuin/2015 7
- 8. PATHOGENESIS AND PATHOLOGY OFARBOVIRUS INFECTION Initial viral replication in Myeloid cell, lymphoid cell or in vascular Primary viremia Reach different tissues and replicates in monocyte, macrophage, endothelial cells, lungs, liver, muscles and brainin vascular endothelium and brain Virus crosses Blood brain barrier through olfactory neurons or cerebral vascular cells Neuronal degeneration (Encephalitis) 2/1/2017 8Dr. Tarek/kuin/2015
- 9. EPIDEMIOLOGY OF ARBOVIRAL DISEASES 2/1/20179Dr. Tarek/kuin/2015
- 10. GENOMIC STRUCTURE OFAN ARBOVIRUS Dr. Tarek/SSMC/2016 10
- 11. DISEASE SYNDROMES PRODUCE BYARBOVIRUS • Three clinical syndromes 1. Undifferentiated fever with or without maculopapular rash 2. Encephalitis2. Encephalitis • Incubation period is 4-21 days • Sudden onset of severe headache, chill and fever, nausea and vomiting, generalized pain • Within 24-48 hours drowsiness, confusion, tremors convulsion and coma develops 3. Haemorrhagic fever 2/1/2017 11Dr. Tarek/kuin/2015
- 12. LABORATORY DIAGNOSIS A. RECOVERYOF VIRUS AND DIRECT DETECTION – Preferable samples are blood, CSF and tissue specimens – Cell culture – Detection of viral RNA and proteins by PCR – Viral antigen detection by immunofluorescence assay or ELISA 2/1/2017 12Dr. Tarek/kuin/2015
- 13. B. SEROLOGY – Preferablesamples are serum and CSF – Antibodies appears few days after onset of illness – Neutralizing antibody and hemagglutination- LABORATORY DIAGNOSIS – Neutralizing antibody and hemagglutination- inhibiting antibodies are detected – Most sensitive method of detection is ELISA – Either virus specific IgM or four fold rise of specific antibody titer is diagnostic 2/1/2017 13Dr. Tarek/kuin/2015
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- 15. CAUSATIVE AGENT – Denguevirus • A single stranded RNA virus of flavivirus family • Enveloped • Spherical in shape• Spherical in shape – Four serotypes-DENV 1 to DENV 4 – Infection with particular serotype is lifelong 15Dr. Tarek/SSMC/2016
- 16. EPIDEMIOLOGY • Dengue isendemic in more than 100 countries • Widely distributed in the tropical region • 50 million or more cases annually • 400,000 cases of DHF annually• 400,000 cases of DHF annually • Risk of developing DHF is 0.2% during first attack • Mortality rate among DHF is 4.1% 16Dr. Tarek/SSMC/2016
- 17. VECTORS • Aedes aegyptispecies mosquito • Aedes albopitus species mosquito 17Dr. Tarek/SSMC/2016
- 18. RESERVOIR • Human isthe urban reservoir • Monkey is the jungle reservoir 18Dr. Tarek/SSMC/2016
- 19. • MOST commonlyby bites of mosquitoes • In rare case: Blood and organ transplantation, mother to offspring • Some people never shows symptoms hence acts as source TRANSMISSION • Some people never shows symptoms hence acts as source • Occurs mainly in the climate of optimal rainfall but periodic epidemic can occur when large number of people are infected in a short period 19Dr. Tarek/SSMC/2016
- 20. FACTORS THAT FAOURS TRANSMISSION •Rapid population growth • Rural-urban migration • Inadequate basic urban infrastructure • Increase in volume of solid waste• Increase in volume of solid waste • Geographical expansion of the mosquito • Increased air travel • Breakdown of vector control measures 20Dr. Tarek/SSMC/2016
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- 22. TYPES OF DENGUEFEVER • Classical dengue fever • Dengue hemorrhagic fever/ dengue shock syndrome 22Dr. Tarek/SSMC/2016
- 23. PATHOGENESIS • UNCOMPLICATED DENGUEFEVER – Virus multiply in the reticuloendothelial cells and vascular endothelium – endothelial cell swelling and perivascular edema– endothelial cell swelling and perivascular edema with mononuclear cell infiltration. 23Dr. Tarek/SSMC/2016
- 24. • DENGUE HAEMORRHAGICFEVER/SHOCK SYNDROME – Formation of virus-antibody complexes by non- neutralizing antibody from primary infection: PATHOGENESIS • Complement activation : – cell recruitment and cytokine release • Activation of macrophage and monocytes – Release of cytokines • Activation of previously sensitized T cells by viral antigen presented by macrophages 24Dr. Tarek/SSMC/2016
- 25. PATHOGENESIS OF DENGUEHEMORRHAGIC FEVER/DENGUE SHOCK SYNDROME • previous infection with one serotype • Passive transfer from • previous infection with one serotype • Passive transfer from • Virus-antibody• Virus-antibody Infection with new serotype • Complement activation • Release of cytokines, vasoactive mediators and procoagulants • Increase vascular • Complement activation • Release of cytokines, vasoactive mediators and procoagulants • Increase vascular transfer from infected mother transfer from infected mother Preexisting Dengue antibody • Virus-antibody complex • Viral entry by non- neutralizing , heterologous, immune enhancing Ab into monocytes and macrophages • Virus-antibody complex • Viral entry by non- neutralizing , heterologous, immune enhancing Ab into monocytes and macrophages • Increase vascular permeability • DIC • Increase vascular permeability • DIC Haemorrhage Shock 2/1/2017 25Dr. Tarek/kuin/2015
- 26. • DENGUE HAEMORRHAGICFEVER/SHOCK SYNDROME – Perivascular edema and widespread effusions into serous cavities such as the pleura PATHOLOGICAL CHANGES serous cavities such as the pleura – Hemorrhages – spleen and lymph nodes show hyperplasia – focal necrosis in the liver – disseminated intravascular coagulation 26Dr. Tarek/SSMC/2016
- 27. CLINICAL MANIFESTATION • Classicaldengue – Incubation period: 4-7 days – Fever is sudden or with prodromal symptoms of malaise, chill, headachemalaise, chill, headache – Fever is saddle back in nature associated with severe bone, muscle and retro-orbital pain – Rash develops on 3rd / 4th day last for 1-5 days – Classical dengue is self limiting 27Dr. Tarek/SSMC/2016
- 28. DENGUE RASH AND TOURNIQUETTEST Maculopapular rash Positive: > 10 petechiae in 1 inch2 28Dr. Tarek/SSMC/2016
- 29. • Dengue hemorrhagicfever/Dengue shock syndrome – Thrombocytopenia – Haemoconcentration CLINICAL MANIFESTATION – Haemoconcentration – Superficial and deep hemorrhage – Circulatory failure 29Dr. Tarek/SSMC/2016
- 30. PHASES OF DHF CRITICALFEBRILECONVALESCENCE Dr. Tarek/SSMC/2016 30 Last: 2-7 days Fever Bone pain Temp. Normal Plasma leak Effusions Shock Hemorrhage 24-48 hours Resolution of plasma leak and recovery 2-4 days
- 31. IMMUNE RESPONSE INDENGUE 31Dr. Tarek/SSMC/2016
- 32. LABORATORY DIAGNOSIS • RT-PCR:Detects viral nucleic acid from acute phase serum roughly during fever (within 5 days) • Serology: – MAC ELISA: Virus specific IgM capture ELISA (after 5 days) – IgG ELISA: Primary and secondary dengue infection – ICT: Detects both IgM and IgG • NS1 ELISA: Detects viral antigens after 1 day of onset • PRNT: Plaque reduction and neutralization test is done to determine infecting serotype in convalescence period Dr. Tarek/SSMC/2016 32
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- 34. • CBC: Leucopenia,Thrombocytopenia, HCT(↑) • USG abdomen: Hepatitis, Ascites LABORATORY DIAGNOSIS 34Dr. Tarek/SSMC/2016
- 35. MANAGEMENT • TREATMENT – Classicaldengue: Symptomatic, Fluid and Nutrition – Haemorrhagic/DSS: • Symptomatic • Adequate IV fluid (Colloidal or Crystalloid) • Fresh frozen plasma • Platelet concentrates or whole blood transfusion • PREVENTION – Mosquito control – Epidemic preparedness and response Dr. Tarek/SSMC/2016 35
- 36. • Unlike Yellowfever and Japanese encephalitis, there is no licensed vaccines for Dengue. • Major hurdles in production of dengue vaccine: – Lack of animal model reproduce human dengue – Presence of multiple serotypes ADVANCES IN DENGUE VACCINE – Presence of multiple serotypes – Risk of immune enhancement in new infection when antibody wanes • Many of the vaccines are in clinical trials 36Dr. Tarek/SSMC/2016
- 37. PROPOSED TYPES OFDENGUE VACCINES • Biologically derived live attenuated dengue vaccine: – Mouse brain-derived dengue virus vaccines – Tissue culture derived live attenuated dengue vaccine • Recombinant live virus vaccines attenuated by engineered mutationsmutations • Inactivated dengue virus vaccine • Recombinant subunit protein vaccines • DNA vaccines • Virus-vectored DENV vaccines 37Dr. Tarek/SSMC/2016
- 38. CHIKUNGUNYA • Virus belongsto Togaviridae family • First isolated in 1953 in Tanzania • Transmitted by mosquito bite• Transmitted by mosquito bite • Most commonly in Africa and Asia , but recently cases isolated in Europe 2/1/2017 Dr. Tarek/kuin/2015 38
- 39. TRANSMISSION OF CHIKUNGUNYA • Mosquitobite: – Ades aegypti : Bite in day time, breeds in household containers – Ades albopictus (Asian tiger mosquito): Human transmission in Asia, Africa and Europein Asia, Africa and Europe • Monkeys and other wild animals can be reservoir of virus • Pregnant women can transmit the virus during delivery, no breast milk transmission 2/1/2017 Dr. Tarek/kuin/2015 39
- 40. GEOGRAPHIC DISTRIBUTION 2/1/2017 Dr.Tarek/kuin/2015 40
- 41. CLINICAL FEATURES OF CHIKUNGUNYAFEVER • Incubation periods: 3-7 days • Fever, headache, muscle pain, headache, joint pain, rash are common symptoms • Hemorrhagic manifestation is not common • Rare incidence of first trimester abortion 2/1/2017 Dr. Tarek/kuin/2015 41
- 42. DIAGNOSIS • Presumptive diagnosisis made on clinical features, recent travel history, epidemiological trend in the particular area • Specimens: Blood, CSFSpecimens: Blood, CSF • TESTS: – Screening: IgM or IgG ELISA – PCR – Histopathology by Immunohistochemistry – Virus culture 2/1/2017 Dr. Tarek/kuin/2015 42
- 43. MANAGEMENT • TREATMENT – Symptomatic –Acetaminophen, Naproxen (Avoid Aspirin) • PREVENTION – No vaccine – Avoid mosquito bite (use insects repellent, nets) – Prevent infected person from going outside for first few days of illness 2/1/2017 Dr. Tarek/kuin/2015 43
- 44. GENERAL PROPERTIES • Singlestranded RNA virus • Genus flavivirus • Closely related to dengue, yellow fever, Japanese• Closely related to dengue, yellow fever, Japanese encephalitis Dr. Tarek/SSMC/2016 44
- 45. TRANSMISSION • Primarily throughmosquito (Aedes species) bites • Maternal-fetal: – Intrauterine – Perinatal– Perinatal • Sexual transmission from infected male partner • Laboratory exposure • Direct contact (in case of heavy viral load) • May be possible through: – Blood transfusion, organ transplant, breast feeding Dr. Tarek/SSMC/2016 45
- 46. THE DISEASE • INCUBATIONPERIOD: • 3-14 days • Viremia ranges from few days to 1 week • Virus remains longer in semen than blood• Virus remains longer in semen than blood Dr. Tarek/SSMC/2016 46
- 47. • Many infectionsasymptomatic • Most common symptoms – Acute onset of fever – Maculopapular rash THE DISEASE Maculopapular rash – Joint pain – Conjunctivitis • Other symptoms include muscle pain and headache Dr. Tarek/SSMC/2016 47
- 48. COMPARISON BETWEEN ZIKA, DENGUEAND CHIKUNGUNYA Dr. Tarek/SSMC/2016 48
- 49. LABORATORY TESTS • Realtime reverse transcriptase-polymerase chain reaction (rRT-PCR) for viral RNA in clinical specimens collected < 7 days (serum) or <14 days (urine) after illness onsetillness onset • Serology for IgM and neutralizing antibodies in serum collected up to 12 weeks after illness onset Dr. Tarek/SSMC/2016 49
- 50. • Plaque reductionneutralization test (PRNT) for presence of virus-specific neutralizing antibodies in paired serum samples LABORATORY TESTS • Immunohistochemical (IHC) staining for viral antigens or RT-PCR on fixed tissues Dr. Tarek/SSMC/2016 50
- 51. SERO-CROSS REACTIVITY • Zikavirus serology (IgM) can be positive due to antibodies against related flaviviruses (e.g., dengue and yellow fever viruses) • Neutralizing antibody testing may discriminateNeutralizing antibody testing may discriminate between cross-reacting antibodies in primary flavivirus infections • Difficult to distinguish infecting virus in people previously infected with or vaccinated against a related flavivirus Dr. Tarek/SSMC/2016 51
- 52. ZIKA AND THEPREGNANCY • Zika virus can pass from a pregnant woman to her fetus during pregnancy or around the time of birth. • Zika infection in pregnancy is a cause of microcephaly and other severe brain defects.and other severe brain defects. • Other problems: – Eye defects, hearing loss, impaired growth, and fetal loss. Dr. Tarek/SSMC/2016 52
- 53. MICROCEPHALY • Head circumference(HC) at birth is less than the 3rd percentile for gestational age and sex. • If HC at birth is not available, HC less than the 3rd• If HC at birth is not available, HC less than the 3rd percentile for age and sex within the first 6 weeks of life. Dr. Tarek/SSMC/2016 53
- 54. TESTING ALGORITHM FORZIKA SUSPECTED INFECTION IN PREGNANT MOTHER Dr. Tarek/SSMC/2016 54
- 55. • There areno vaccine or medicine Zika. • Treat the symptoms of Zika • Rest, Drink fluids to prevent dehydration • Take acetaminophen to reduce fever and pain MANAGEMENT • Take acetaminophen to reduce fever and pain • Do not take aspirin or other non-steroidal anti- inflammatory drugs (NSAIDS) until dengue can be ruled out to reduce the risk of bleeding. Dr. Tarek/SSMC/2016 55
- 56. REFERENCES • Jawetz, Melnick,Adelberg. Medical Microbiology. 25th ed. Lange publication; 2010. • Kenneth J.R, C. George Ray, editors. Sherris Medical Microbiology.4th edition. McGraw-Hill, Inc; 2004. • Alan L. Rothman. Current topics in Microbiology and• Alan L. Rothman. Current topics in Microbiology and Immunology, vol 336: Springer-Verlag Berlin Heidelberg, 2010. • http://www.who.int/csr/disease/dengue/impact/en/ • http://www.cdc.gov/Dengue/epidemiology/index.html • http://kpkesihatan.com/2015/04/ 56Dr. Tarek/SSMC/2016
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