Dengue & RF fever (internal medicine) .pptx

Dengue & RF fever

1. Dengue fever And Rift valley fever Dr. Nshwan Mansoor 1

2. Dengue fever A febrile illness caused by a flavi-virus transmitted by mosquitoes. It is endemic in Asia, the Pacific, Africa and the Americas. Dengue is the most rapidly spreading mosquito-borne viral illness. The principal vector is the mosquito Aedes aegypti. The four serotypes of dengue virus, all producing a similar clinical syndrome; type-specific immunity is life-long but immunity against the other serotypes lasts only a few months. Dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) occur in individuals who are immune to one dengue virus. Prior immunity results in increased uptake of virus by cells increased T-cell activation with resultant cytokine release, causing capillary leak and disseminated intravascular coagulation. Previously, dengue most frequently in those 16–45 years of age or older, in whom severe organ dysfunction is more common. Other epidemiological changes include the spread of dengue into rural communities and greater case fatality in women . Dr. Nashwan Mansoor 2

3. Dengue fever Clinical features :- Many cases of dengue infection are asymptomatic in children. Clinical disease presents with undifferentiated fever termed dengue-like illness. When dengue infection occurs with characteristic symptoms or signs it is termed ‘dengue’. A rash frequently follows the initial febrile phase as the fever settles. Laboratory features include:- Leucopenia, neutropenia thrombocytopenia. Elevated alanine aminotransferase (ALT) or aspartate aminotransferase (AST). Many symptomatic infections run an uncomplicated course but complications or a protracted convalescence may ensue. Warning signs justify intense medical management and monitoring for progression to severe dengue. Atypical clinical features of dengue are increasingly common, especially in infants or older patients. Dr. Nashwan Mansoor 3

4. Dengue fever Clinical features :- Along with DHF or DSS, are recognized as features of severe dengue in the 2015 case definition. The period 3–7 days after onset of fever is termed the ‘critical’ phase, during which signs of DHF or DSS may develop. In mild forms:- Petechiae occur in the arm when a blood pressure cuff is inflated to a point between systolic and diastolic blood pressure and left for 5 minutes (the positive ‘tourniquet test’) a non-specific test of capillary fragility and thrombocytopenia. DHF:- May present with :- Minor (Petechiae, ecchymosis, epistaxis). Major (gastrointestinal or vaginal) haemorrhage. Cerebrovascular bleeding may be a complication of severe dengue. Dr. Nashwan Mansoor 4

5. Dengue fever Clinical features :- Clinical Case Definition for Dengue Hemorrhagic Fever 4 Necessary Criteria: Fever, or recent history of acute fever. Hemorrhagic manifestations. Low platelet count (100,000/mm3 or less). Objective evidence of “leaky capillaries:” Elevated hematocrit (20% or more over baseline). Low albumin. Pleural or other effusions Dr. Nashwan Mansoor 5

6. Dengue fever Clinical features :- DSS:- Develops as the extent of capillary leak increases, with:- A raised hematocrit. Tachycardia. Hypotension. Pleural effusions. Ascites. Clinical Case Definition for Dengue Shock Syndrome:- 4 criteria for DHF + Evidence of circulatory failure manifested indirectly by all of the following:- Rapid and weak pulse. Narrow pulse pressure ( < 20 mm Hg) OR hypotension for age. Cold, clammy skin and altered mental status. Frank shock is direct evidence of circulatory failure. Dr. Nashwan Mansoor 6

7. Dengue fever Diagnosis :- In endemic areas, mild dengue must be distinguished from other viral infections. The diagnosis can be confirmed by seroconversion of IgM or a fourfold rise in IgG antibody titres. Serological tests may detect cross-reacting antibodies from infection or vaccination against other flaviviruses. Isolation of dengue virus or detection of dengue virus RNA by PCR. (ELISA) kits to detect the viral antigen. Dr. Nashwan Mansoor 7

8. Dengue fever Management and prevention :- Treatment is supportive, emphasizing fluid replacement and appropriate management of shock and organ dysfunction, which is a major determinant of morbidity and mortality. With intensive care support, mortality rates are 1% or less. Aspirin should be avoided due to bleeding risk. Glucocorticoids have not been shown to help. No existing antivirals are effective. Breeding places of Aedes mosquitoes should be abolished and the adults destroyed by insecticides. A recently licensed vaccine is available. Dr. Nashwan Mansoor 8

9. Rift valley fever Dr. Nashwan Mansoor 9

10. Rift valley fever Acute febrile viral disease. Affecting animals & humans . Causes influenza-like illness. May lead to high morbidity, mortality & economic loss. Outbreaks in the Last Half Century:- 2000-2001 in Yemen and Saudi Arabia. Dr. Nashwan Mansoor 10

11. Rift valley fever Mode of Transmission:- Mosquitoes . Other blood suckling insects. Contact with blood or other body fluids of infected animals. Consumption of infected milk. Contact with blood or other body fluids of infected humans in late stages of disease. Airborne transmission. Inoculation through broken skin. Target:- Liver: focal necrosis. RBCs: haemagglutination . Brain: necrotic encephalitis. Dr. Nashwan Mansoor 11

12. Rift valley fever Clinical Picture :- Dr. Nashwan Mansoor 12 Human Host Non-Human Host Incubation period of 2-6 days. Asymptomatic. Flu-like illness. Abdominal pain. Photophobia. Recovery in 2-7days. Fever. Hepatitis. Abortion. Death:- Adults: 10-30%. Neonates: 100%.

13. Rift valley fever Complications of RVF :- Dr. Nashwan Mansoor 13 3) Haemorrhagic fever 2) Meningoencephalitis 1) Ocular Lesions Presentation:- Hemorrhagic phenomenon. Lesions:- Acute fulminant hepatitis. DIC. Hemolytic anemia. CRF: 50 %. Presentation:- Severe headache. Vertigo. Seizures. Coma. Presentation:- Localized pain. Blurred vision. Loss of vision. Lesions:- Macular lesions. Retinitis. Retinal detachment.

14. Rift valley fever High Risk Groups:- People who sleep outdoors at night. Slaughter house workers, butchers veterinarians and others who handle blood, other body fluids or tissues of infected animals. Doctors and nurses in contact with infected cases at late stages of the disease. Laboratory technicians. Travelers visiting epidemic areas. Diagnosis of RVF:- Antibody detection:- ELISA. EIA. Virus detection:- Virus isolation. Antigen detection. PCR. Dr. Nashwan Mansoor 14

15. Rift valley fever Prevention & Control:- 1) Animal:- Vaccination of unaffected animals:- Live attenuated vaccine. Killed vaccine. Notification of affected animals. Application of safe insecticides to eradicate blood suckling insects . Periodic surveillance of susceptible animals to assess immune status . Application of quarantine measures for testing of imported animals. Rapid burial of dead bodies. 2) Vector:- Removal of stagnant water . Weekly treatment of water collections using insecticides. Application of insecticides every other day in all gardens. Removal of objects that can act as possible water containers. Dr. Nashwan Mansoor 15

16. Rift valley fever Prevention & Control:- 3) Humans:- A) General Measures:- Sleeping indoors. Using bed nets during sleep. Putting screens on windows. Wearing clothes that protects whole body. Applying mosquito repellents. Using spray on clothes. Avoiding peaks of mosquito activity. Avoiding presence near vegetation's in the evening. Avoiding direct contact with animals . Washing hands after contact with animals, their blood or other body fluids. Avoid drinking raw milk . Dr. Nashwan Mansoor 16

17. Rift valley fever Prevention & Control:- 3) Humans:- B) Community Measures:- Health education. Epidemiologic research program. Active disease surveillance. Check measures at air, sea and land entry points. C) Occupational Measures:- Wearing masks, gloves, gowns and other barriers according to infected host’s condition . Laboratory samples should be handled by trained staff . Application of water, soap and antiseptic solution on exposed parts. Application of copious water and eye wash solution on exposed conjunctiva. Dr. Nashwan Mansoor 17

18. Rift valley fever Management of Suspected Cases :- Notification. Ascertainment of cases. Identification, screening and surveillance of contacts. Recommended Investigations:- CBC. Urea and Creatinine. AST, ALT, ALP, Bilirubin . Albumin. PT & PTT. LDH & CPK. Hepatitis A IgM & IgG, HBsAg, HBcAB , HCV Ab. RFV serology & viral culture. Dr. Nashwan Mansoor 18

19. Rift valley fever Management of Suspected Cases :- Management of unhospitalised Patients:- Isolation at home. Contacts should wear masks, gloves and protective clothes. Safe disposal of patients linens & clothes. Close follow-up for 6 weeks. Indications For Hospitalisation:- Shock. Decreased urine output. AST & ALT > 200U/ mL. Bilirubin>100 mol/L. Thrombocytopenia< 100,000/mm3. Anaemia< 8gm/dL. Creatinine>150mol/L. Confusion or other CNS manifestation. Evidence of DIC. Dr. Nashwan Mansoor 19

20. Rift valley fever Management of Suspected Cases :- Management of Hospitalised Patients:- General Supportive Measures. Isolation in negative airway pressure room. Safe disposal of soiled linens. Safe disposal of solid medical waste. Safe sewage disposal . Ribavirin, Interferon, Immune Modulators & Convalescent Phase Plasma give promising results. Introduction to ICU or hemodialysis unit if indicated. Hospital discharge after:- Improvement in general status. Decline in liver symptoms. Recovery from DIC. Follow-up in ophthalmology and medical clinics for 6 weeks . Safe burial practice for dead cases. Dr. Nashwan Mansoor 20