MICR 454L Emerging and Re-Emerging Infectious Diseases Lecture 12: Ebola Virus, Dengue virus (Reading:Emerging Viruses) Dr. Nancy McQueen & Dr. Edith Porter Overview Ebola Virus Dengue Virus Brief history Morphology Genome Replication cycle Diseases Pathogenesis Diagnosis Treatment Prevention Threats Ebola Virus Ebola Virus - Brief History In 1976 two epidemics of hemorrhagic fever occurred simultaneously in Zaire and Sudan. Over 500 cases were reported with a mortality rate of 88% in Zaire and 54% in Sudan A new virus that was isolated as the causative agent was named after the Ebola River in Zaire. Subsequent outbreaks occurred in Sudan in 1977 and 1979. In 1994 the first Ebola case was reported in West Africa. In 1989 an outbreak occurred in cynomolgus monkeys imported from the Philippines to a facility in Reston, Virginia . Luckily that species does not appear to be pathogenic to humans Ebola Virus - Brief History Sporadic outbreaks, most in equatorial Africa, continue to occur Endemic in Sudan, Zaire, and the Ivory Coast. Very pathogenic for monkeys and apes - argues against these animals as the natural host. Recent studies - virus can replicate in fruit and insecteating bats without any ill effects to the bat. Thus, bats may be the natural reservoir for the virus. Ebola Virus - Taxonomy Ebola virus belongs to the family Filoviridae, genus Ebolavirus There are four identified subtypes, three of which infect humans Filamentous, helical, enveloped virus Linear SS, - RNA genome Ebola Virus Replication Cycle Budding from the plasma membrane Penetration via receptor mediated endocytosis mRNA synthesis and genome replication in the cytoplasm Fusion with endosomal membrane (uncoating) Ebola Virus – Transmission to Humans How the virus first appears in a human at the start of an outbreak has not been determined. ? contact with an infected animal. After the first case-patient in an outbreak setting is infected, virus can be transmitted via: Direct contact with the blood and/or secretions of an infected person. Contact with objects, such as needles, that have been contaminated with infected secretions. Sexual contact Aerosol transmission has been documented in non-human primates, but not in humans Ebola Virus Diseases/Pathogenesis Incubation - 2 to 21 days Symptoms abrupt - characterized by fever, headache, joint and muscle aches, sore throat, and weakness followed by diarrhea, vomiting, and stomach pain rash, red eyes and hiccups may also occur dendritic cells and macrophages initially infected followed by hepatocytes, and, in latter stages, endothelial cells. virus evades host defenses by producing proteins (vp24, vp35) that interfere with interferon signaling pathway. Ebola Virus – Pathophysiology of the Disease Clinical infection in human and nonhuman primates is associated with rapid and extensive viral replication in all tissues. A viral glycoprotein, sGP binds to a neutrophil-specific receptor and inhibits early neutrophil activation. Viral replication is accompanied by widespread and severe focal necrosis. The most severe necrosis occurs in the liver. sGP also may be responsible for the profound lymphopenia that characterizes Ebola infection A second viral glycoprotein binds to endothelial cells but not to neutrophils, allowing Ebola virus to invade, replicate in, and destroy endothelial cells. Ebola Virus - Pathophysiology of the Diseases Destruction of endothelial surfaces causes the vessels to leak and bleed. Destruction of the endothelial surfaces can lead to disseminated intravascular coagulation (DIC), and this, combined with the liver destruction may contribute to the hemorrhagic manifestations that characterize Ebola infections. The two major factors in Ebola virus pathogenesis are the impairment of the immune response and vascular dysfunction. Death results from liver damage and dysfunction, shock, and the DIC which leads to internal and external bleeding mortality rate ranges from 30-90% Ebola Hemorrhagic Fever Ebola Virus- Diagnosis Serology Molecular tests ELISA RT-PCR Virus isolation - Must use biocontainment level IV facility! Ebola Virus - Treatment There is no standard treatment for Ebola hemorrhagic fever (HF). Patients receive supportive therapy balancing the patient’s fluids and electrolytes, maintaining their oxygen status and blood pressure, and treating them for any complicating infections. Ribavirin treatment has been tried with little success. Ebola Virus - Prevention No vaccine is currently available, but many are in development Practical viral hemorrhagic fever isolation precautions, or barrier nursing techniques must be used. These techniques include the wearing of protective clothing, such as masks, gloves, gowns, and goggles the use of infection-control measures, including complete equipment sterilization the isolation of Ebola HF patients from contact with unprotected persons. direct contact with the body of a deceased patient should be prevented. Ebola Virus - Threats Sporadic epidemics continue to occur challenge of developing additional diagnostic tools to assist in early diagnosis of Ebola HF challenge of conducting ecological investigations of Ebola virus and its possible reservoir (bats). challenge to determine how the virus is transmitted to humans must be acquired to prevent future outbreaks effectively. Use as bioterrorism weapon Kills too quickly? Aerosol spread? Take Home Message Ebola virus belongs to the family Filoviridae Enveloped with linear SS, - RNA genome Reservoir appears to be bats Virus targets dendritic cells, macrophages, hepatocytes, endothelial cells Virus impairs immune function in several ways Liver and endothelial cell destruction DIC internal and external bleeding High mortality rate Diagnosis via serology, molecular tests, virus isolation (level IV biocontainment) Treatment - supportive care Vaccines in development Dengue Virus Brief History The first cases of Dengue Fever (DF) were recorded in 1779 in Batavia, Indonesia, and Cairo In 1780, there was an epidemic reported in Philadelphia, PA. For the past 200 years, pandemics have been recorded in tropical and subtropical climates at 10 to 30 year intervals. Although DF is not a new disease, it can be classified as an emerging disease. Since 1945, the number of reported cases of DF surged because of increased urbanization and travel Dengue Virus- Classification Is in the family Flaviviridae, genus flavivirus Belong to Group B arboviruses (arthropod borne animal viruses) Transmitted by female Aedes aegypti mosquitoes Has 4 serotypes (DEN-1, 2, 3, 4) Enveloped, single-stranded + RNA genome Dengue Virus Replication Cycle Budding from ER exocytosis mRNA synthesis and genome replication in the cytoplasm Transmission of Dengue Virus by Aedes aegypti Mosquito feeds / acquires virus Mosquito refeeds / transmits virus Intrinsic incubation period Extrinsic incubation period Viremia Viremia 0 5 Illness Human #1 8 12 16 DAYS Human #2 20 24 Illness 28 Replication and Transmission of Dengue Virus 1 1. Virus transmitted to human in mosquito saliva 2 4 2. Virus replicates in target organs 3. Virus infects white blood cells and lymphatic tissues 4. Virus released and circulates in blood 3 Replication and Transmission of Dengue Virus 5. Second mosquito ingests virus with blood 6. Virus replicates in mosquito midgut and other organs, infects salivary glands 7. Virus replicates in salivary glands 6 7 5 Diseases Undifferentiated fever Classic dengue fever Dengue hemorrhagic fever Dengue shock syndrome Undifferentiated Fever most common manifestation of dengue 87% of students infected are either asymptomatic or only mildly symptomatic Classic Dengue Fever Fever Headache Muscle and joint pain Nausea/vomiting Rash (petechiae) Hemorrhagic manifestations Encephalitis Decreased level of consciousness: lethargy, confusion, coma Seizures Nuchal rigidity Paresis (slight paralysis) Petechiae Dengue Hemorrhagic Fever (DHF) Skin hemorrhages: petechiae, purpura, ecchymoses Gingival bleeding Nasal bleeding Gastro-intestinal bleeding: hematemesis, melena (dark stools), hematochezia (bloody stools) Hematuria Increased menstrual flow 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 Pleural Effusion Index PEI = A/B x 100 B A Vaughn DW, Green S, Kalayanarooj S, et al. Dengue in the early febrile CENTERS FOR DISEASE CONTROL phase: viremia and antibody responses. J Infect Dis 1997; 176:322-30. AND PREVENTION 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 Shock is direct evidence of circulatory failure Risk Factors For Dengue Hemorrhagic Fever (DHF) Second infection with a different serotype Virus strain Virus serotype Due to pre-existing, non-neutralizing anti-dengue antibody Presence of maternal antibody to a different serotype DHF risk is greatest for DEN-2, followed by DEN-3, DEN-4 and DEN-1 Host genetics Age Higher risk in locations with two or more serotypes circulating simultaneously at high levels (hyperendemic transmission) Hypothesis on Pathophysiology of DHF Persons who have experienced a dengue infection develop serum antibodies that can neutralize the dengue virus of that same (homologous) serotype. Dengue 1 virus Neutralizing antibody to Dengue 1 virus Non-neutralizing antibody Complex formed by neutralizing antibody and virus Hypothesis on Pathophysiology of DHF In a subsequent infection, the pre-existing heterologous nonneutralizing antibodies form complexes with the new infecting virus serotype, but do not neutralize the new virus. Dengue 2 virus Non-neutralizing antibody to Dengue 1 virus Complex formed by non-neutralizing antibody and virus Hypothesis on Pathophysiology of DHF Antibody-dependent enhancement of virus uptake - Dengue virus, complexed with non-neutralizing antibodies binds to Fc receptor and enters monocytes/macrophages (Note - This entry into monocytes or macrophages is not dependent on the cell having the receptor to which the virus must normally bind for Fc receptor entry.) Fc region Dengue 2 virus Non-neutralizing antibody Complex formed by non-neutralizing antibody and Dengue 2 virus Hypothesis on Pathophysiology of DHF Hemorrhagic manifestations that characterize DHF and DSS due to: Infected monocytes/macrophages release of vasoactive mediators, resulting in increased vascular permeability. circulating dengue antigen-antibody complexes that activate complement, resulting in the release of vasoactive mediaters. the process of immune elimination of infected cells, that releases proteases and lymphokines that activate complement, coagulation cascades (leads to DIC) and vascular permeability factors. Diagnosis ELISA Virus isolation Cell culture Mosquito inoculation Fluorescent antibody test RT-PCR Diagnosis -Tourniquet Test Inflate blood pressure cuff to a point midway between systolic and diastolic pressure for 5 minutes Positive test: 20 or more petechiae per 1 inch2 (6.25 cm2) Pan American Health Organization: Dengue and Dengue Hemorrhagic Fever: Guidelines for Prevention and Control. PAHO: Washington, D.C., 1994: 12. Positive Tourniquet Test Treatment Fluids Rest Antipyretics (avoid aspirin and non-steroidal anti-inflammatory drugs) Monitor blood pressure, hematocrit, platelet count, level of consciousness Avoid invasive procedures when possible Unknown if the use of steroids, intravenous immune globulin, or platelet transfusions to shorten the duration or decrease the severity of thrombocytopenia is effective Patients in shock may require treatment in an intensive care unit Mosquito Barriers Only needed until fever subsides, to prevent Aedes aegypti mosquitoes from biting patients and acquiring virus Keep patient in screened sickroom or under a mosquito net Prevention No licensed vaccine at present Effective vaccine must be tetravalent Field testing of an attenuated tetravalent vaccine currently underway Effective, safe and affordable vaccine will not be available in the immediate future Threats Dengue virus causes about 100 million cases of acute febrile disease annually, including more than 500,000 reported cases of DHF/DSS and up to 50,000 deaths. Currently, dengue is endemic in 112 countries. From 1977 to 2004, a total of 3,806 suspected cases of imported dengue were reported in the United States. Dengue epidemic in Brazil in April, 2008 killed 106 but now seems to be abating Take Home Message Dengue virus is in the family Flaviviridae Enveloped, single-stranded + RNA genome 4 serotypes Transmitted by female Aedes aegypti mosquito Causes undifferentiated fever, dengue fever, dengue hemorrhagic fever (skin hemorrhages, low platlet count, leaky capillaries) , dengue shock syndrome ( circulatory collapse and shock) Risk factors for DHF include secondary infection with a different serotype - due to non-neutralizing antibodies Hemorrhagic manifestations due to increased vascular permeability and coagulation activation Diagnosis includes tourniquet test Treatment is rest, fluids, antipyretics Tetravalent vaccine in development Resources The Microbial Challenge, by Krasner, ASM Press, Washington DC, 2002. Brock Biology of Microorganisms, by Madigan and Martinko, Pearson Prentice Hall, Upper Saddle River, NJ, 11th ed, 2006. Microbiology: An Introduction, by Tortora, Funke and Case; Pearson Prentice Hall; 9th ed, 2007. Fundamentals of Molecular Virology, by Nicholas Acheson; Wiley and Sons; 2007 Human Virology by Collier and Oxford, Oxford University Press; 2nd edition, 2000. www.cdc.gov http://www.defenseindustrydaily.com/images/MISC_Ebola_Patient.jp g http://www.kcom.edu/faculty/chamberlain/website/lectures/lecture/IM AGE/HEMFEVM.GIF http://www.cdc.gov/ncidod/dvbid/dengue/index.htm#current Resources www.cdc.gov http://www.hepcprimer.com/images/cutmodel-with-text.gif