Yellow Fever, Dengue Virus & Zika Virus.pptx

this is a presentation on the 3 viral infections that are found in Zambia

1. Y ellow Fever, Dengue & Zika Virus BORNFACE KAFUTE, BSc HB, MBChB

2. YELLOW FEVER, DENGUE and ZIKA VIRUS are Arbovirus (thus cause Arboviral diseases). Transmitted by aedes aegypti (female ) Affects humans and higher vertebrates Can cause Viral hemorrhagic fevers They belong to a family of viruses known as Flaviviridae under the Genus called Flaviviruses . Introduction to the disease

3. Positive sense single stranded RNA Icosahedral capsid with C proteins surround the Genome Enveloped with lipid bi-layer that has M and E Proteins 40-50nm  in diameter . Morphology And Genome

4. Dengue

5. Pathogenesis The transmission cycle of dengue virus by the mosquito Aedes aegypti begins with a dengue-infected person. This person will have virus circulating in the blood-a viremia that lasts for about five days. During the viremic period, an uninfected female Aedes aegypti mosquito bites the person and ingests blood that contains dengue virus.

6. Epidemiology Particularly Africa, the Americas, the Eastern Mediterranean, South Asia, South-east Asia and the Western Pacific, the Middle East, Africa, the Far East, and the Caribbean Islands These viral agents are widespread throughout the world

7. Clinical Presentation Characterized by high fever, erythematous rash , severe pain in the back eye muscles, bones and joints. Also mild bleeding such as nose or gum bleeding.

8. Host Immune Response Innate and Adaptive response is the same.However subsequent infections with other serotypes increases risk of developing severe Dengue disease, most likely by antibody dependant enhancement (ADE), enhancing antibodies that do not neutralize the virus rather enhance viral entry into host cells.

9. Diagnosis serological tests and molecular assays . Detection of NS1 antigen in serum during the early phase of illness is common. IgM and IgG antibodies are detected using ELISA. Molecular methods like PCR are utilized for viral RNA detection. Serological testing

10. Treatment & Prevention treatment focuses on supportive care to manage symptoms, as there is no specific antiviral treatment. Prevention primarily involves vector control measures to reduce mosquito populations and vaccine development efforts .

11. Yellow Fever

12. Pathogenesis Female mosquito bites and intra-dermally inoculates an individual with 1000-100,000 viral particles Multiply locally in dendritic cells and spread to lymph nodes Primary replication occurs in monocytes/macrophages and large histiocytes Spreads lymphatically and seeds other organs

13. Pathogenesis Liver, spleen and lymph nodes are sites of large viral production During viremic phase, infected human can transmit to blood-feeding mosquito ( Viremic Phase = First 3-6 Days ) Large viral loads cause liver damage (mid-zone) and (condensed nucleus chromatin) Councilman bodies

14. Epidemiology it is not reported in India. Occurs in tropical and subtropical areas in Africa,south America and Caribbean.

15. Clinical Presentation Acute Phase: The initial symptoms of yellow fever are nonspecific and may include fever, muscle pain, headache, and loss of appetite. Patients may also experience nausea, vomiting, and weakness during the acute phase of the illnesses.   2. Toxic Phase:   High fever, jaundice , dark urine due to liver involvement, abdominal pain, and bleeding manifestations.

16. complications Multi-organ dysfunction Hemorrhage Neurological complicationmonia or sepsis.   Long-term complications: including post-viral fatigue syndrome, cognitive impairment, and hepatotoxicity.

17. Host Immune Response Innate immune response:upon infection, antigen presenting cells such as macrophages recognize the virus through pattern recognition receptors initiating the inflammatory response.There is release of cytokines and interferon.Activation of immune cells, macrophages and neutrophils which engulf viral particles.Natural killer cells destroy virus infected cells directly . Adaptive immune response:There is activation of T helper cells and differentiation to Th1 for cell mediated immunity, Th2 for humoral response and Th17.Tcytotoxic cells clears the infection and there is production of serotype specific antibodies.Memory B and T cells are formed.Lifelong immunity is serotype specific.

18. Diagnosis Laboratory diagnosis involves detecting viral Serological tests like -ELISA are used to detect specific IgM antibodies. PCR

19. Treatment & Prevention For yellow fever, treatment mainly involves supportive care as there are no specific antiviral therapies. Vaccination is the most effective means of prevention.

20. ZIKA VIRUS

21. Pathogenesis Mosquito-borne flaviviruses are thought to replicate initially in dendritic cells near the site of inoculation . Then spread to lymph nodes and the bloodstream. Although flaviviral replication is thought to occur in cellular cytoplasm, one study suggested that Zika Virus antigens could be found in infected cell nucleus

22. Epidemiology Zika is now distributed in Central and South America, the Caribbean, Cape Verde (Africa), Singapore and Vietnam (Southeast Asia), the Pacific Island, Puerto Rico, and all states of the United States.

23. Clinical Presentation fever rash joint pain muscle pain headache conjunctivitis These symptoms last for 2 to 7  days

24. Host Immune Response Zika virus infection often results in a mild immune response in healthy individuals, but in pregnant women, it can lead to complications such as microcephaly due to immune-mediated mechanisms.

25. Diagnosis detecting viral RNA or specific antibodies. RT-PCR Serological tests such as IgM and IgG  ELISA

26. Treatment & Prevention Treatment is primarily supportive, focusing on managing symptoms such as fever and pain. Prevention involves avoiding mosquito bites, particularly for pregnant women to prevent congenital Zika syndrome, and efforts to control mosquito populations. Additionally, research into vaccines continues.

27. THANK YOU