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Viral Hemorrhagic Fever CHAPTER Viral Hemorrhagic Fever 11 Debasis Chakrabarti INTRODUCTION • Human cases or outbreaks of hemorrhagic fevers Viral hemorrhagic fevers (VHFs) refer to a group of caused by these viruses occur sporadically and illnesses that are caused by several distinct families of irregularly. The occurrence of outbreaks cannot be viruses. In general, the term “viral hemorrhagic fever” is easily predicted. used to describe a severe multisystem syndrome (multiple With a few noteworthy exceptions, there is no cure or organ systems in the body are affected). Characteristically, established drug treatment for VHFs. the overall vascular system is damaged, and the body’s ability to regulate itself is impaired. These symptoms are General characteristics of these viral families can be found often accompanied by hemorrhage (bleeding). While some in this table below. types of hemorrhagic fever viruses can cause relatively TRANSMISSIONS mild illnesses, many of these viruses cause severe, life- Viruses causing hemorrhagic fever are initially threatening diseases. transmitted to humans when the activities of infected ETIOLOGY reservoir hosts or vectors and humans overlap. Some A wide range of viruses can cause viral hemorrhagic fever viruses that cause hemorrhagic fever can spread from (VHF) and hence are designated as hemorrhagic fever one person to another, once an initial person has become viruses. infected. Ebola, Marburg, Lassa and Crimean-Congo hemorrhagic fever viruses are examples. This type of • The family Arenaviridae include the viruses secondary transmission of the virus can occur directly, responsible for Lassa fever and Argentine, Bolivian, through close contact with infected people or their body Brazilian and Venezuelan hemorrhagic fevers. fluids. It can also occur indirectly, through contact with • The family Bunyaviridae include the members objects contaminated with infected body fluids. For of the Hantavirus genus that cause hemorrhagic example, contaminated syringes and needles have played fever with renal syndrome (HFRS), the Crimean- an important role in spreading infection in outbreaks of Congo hemorrhagic fever (CCHF) virus from the Ebola hemorrhagic fever and Lassa fever. Nairovirus genus, and the Rift Valley fever (RVF) PATHOPHYSIOLOGY virus from the Phlebovirus genus. The primary defect in patients with viral hemorrhagic • The family Filoviridae includes Ebola virus and fever (VHF) is that of increased vascular permeability Marburg virus. Finally, the family Flaviviridae due to multiple cytokines activations. Hemorrhagic includes dengue, yellow fever, and two viruses in fever viruses have an affinity for the vascular system, the tick-borne encephalitis group that cause VHF: leading initially to signs such as flushing, conjunctival Omsk hemorrhagic fever virus and Kyasanur injection, and petechial hemorrhages, usually associated Forest disease virus. with fever and myalgias. Later, frank mucous membrane hemorrhage may occur, with accompanying hypotension, COMMON CHARACTERISTICS shock, and circulatory collapse. • They are all RNA viruses, and all are covered, or enveloped, in a fatty (lipid) coating. Inadequate or delayed immune response to these novel viral antigens may lead to one hand rapid development • Their survival is dependent on an animal or insect of overwhelming viremia and other hand pronounced host, called the natural reservoir. macrophage activation with extensive damage of affected • The viruses are geographically restricted to the organs. Hemorrhagic complications are multifactorial and areas where their host species live. are related to hepatic damage, consumptive coagulopathy, and primary marrow injury to megakaryocytes. • Humans are not the natural reservoir for any of these viruses. Hepatic involvement varies with the infecting organism and is at times seen with Ebola, Marburg, RVF, CCHF, and • Humans are infected when they come into contact yellow fever. Renal failure with oliguria is a prominent with infected hosts. However, with some viruses, feature of HFRS seen in Hantavirus infection and may after the accidental transmission from the host, be seen in other VHFs as intravascular volume depletion humans can transmit the virus to one another. becomes more pronounced. Bleeding complications are 46 Table 1: Viruses causing Hemorrhagic Fever Virus Diseases Incubation Case Case Natural Usual Target Population Period Infection Fertility Distribution Source of (Days) ratio Rate Human Infection Arenaviridae: Lassa Fever 5-16 Commonly 15% West Africa Rodent All ages Both Arena virus mild sexes infection Argentine 7-14 >1/2 15-30% South Rodent All ages Both sex HF infections America result in Disease Bolivian HF 9-15 >1/2 15-30% South Rodent Countryside:Men. infections America Village: All age INFECTION result in both sexes Disease Venezuelans 7-14 >1/2 15-30% South Rodent All ages both HF infections America sexes result in Disease Bunia viridae Rift valley 2-5 1:100 50% Sub-Saharan Mosquito All age both i. Phlebo Fever Africa, sex, Men virus Madagaskar, more exposed, Egypt Liver disease Predisposed ii. Nairo Crimean- 3-22 ≥1:5 15-30% Europe, Asia, Tick All age both virus Congo HF Africa sex, Men more exposed iii. Hanta HF with 9-35 Hantan Hantan Worldwide Rodent Adult male more virus renal > 1:1.25 5-15% depending prone syndrome Puumala Puumala on rodent 1:20 <1% reservoir Hanta virus 7-28 Very high 40-50% Americas Rodent Adult male more Pulmonary prone syndrome Filoviridae Marburg 3-16 High 25-90% Sub Saharan Unknown All ages both sex, Filovirus and Ebola Africa Child less exposed virus Flavivirus Yellow fever 3-6 1:2 – 1:20 20% Africa, South Mosquito All ages both America sexes adult more exposed, preexisting flaviirus immunity may cross protect New New Arena Luzo virus 2 weeks Very high Highly Lusaka Rodent, All ages both virus (Discovered fatal (Zambia), Bat sexes in 2008) Johannesburg (South Africa) New Flavi Alkhumra Few weeks Very high 25% Saudi Arabia Sheep, Al ages both sexes virus hemorrhagic Goat, fever Rodent. Mosquito particularly prominent with Ebola, Marburg, CCHF, and • Avoid intramuscular injections and the use of 47 the South American arena viruses. aspirin or other anticoagulants. COMMON CLINICAL FEATURES • Minimize invasive procedures because of the risk Although clinical features vary somewhat for the various associated with viral transmission from sharp hemorrhagic fever viruses, the clinical presentations objects overlap substantially. All of the agents cause a febrile Infection control measures include the following: prodrome associated with varying degrees of prostration; other notable features include the following. • Prevent nonessential staff and visitors from entering the room • Bleeding manifestations occur in variable proportions of patients (eg, in about 30% of patients • All staff entering the room should wear gloves and gowns with Ebola or Marburg hemorrhagic fever and in CHAPTER 11 only about 1% of patients with Rift Valley fever). • Persons coming within 3 feet of the patient should • A maculopapular rash may be noted early in the wear face shields or surgical masks with eye clinical course in some forms of VHF (notably in • protection (including side shields); use HEPA filter Ebola and Marburg hemorrhagic fevers) masks if patients have prominent respiratory, GI, • Severe exudative pharyngitis is a characteristic or hemorrhagic symptoms. early feature of Lassa fever. • If large amounts of blood or other body fluids • Several agents cause meningoencephalitis in are present in the environment, use leg and shoe addition to VHF (eg, Rift Valley fever, Kyasanur coverings. Forest disease, Omsk hemorrhagic fever viruses). • Before exiting the room, discard all used protective • Jaundice may be a prominent feature in some barriers and clean shoes with a hospital disinfectant infections (eg, Ebola and Marburg hemorrhagic or solution of household bleach. fevers, Lassa fever, Rift Valley fever, yellow fever). • If possible, use an anteroom for putting on and INVESTIGATIONS removing protective barriers and for storing supplies. There may be leucopenia, thrombocytopenia with elevated hepatic enzymes, raised prothombin time, activated No specific antiviral therapy is available for Ebola or partial thromboplastin time and fibrin degradation Marburg virus infection. The use of convalescent serum product in patients with hemorrhages and hepatopathy. (ie, sera from patients who have survived infection) is suggested as a possible therapy. Specific viral diagnosis can be made using serologic tests, including enzyme-linked immunosorbent assay (ELISA) Lassa fever and HFRS due to Hantavirus infection and polymerase chain reaction. Difficult cases may require have been treated effectively with intravenous and oral tissue cultures. During the 2000-2001 Ebola outbreak in ribavirin. Because of this, ribavirin has been recommended Uganda, reverse transcriptase-PCR (RT-PCR) emerged as as a potential treatment for other arena viruses and bunya a very effective means for detecting Ebola virus in patient viruses. Treatment is most effective when given early serum, plasma, and whole blood. Report all suspected in the clinical course. Ribavirin also is recommended cases of viral hemorrhagic fever (VHF) immediately to for post exposure prophylaxis. Other potential antiviral local and state public health departments and to the CDC. therapies against Lassa fever include novel benzimidazole compounds such as ST-193 and other related heterocyclic Because of the need for specialized microbiologic compounds.
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