* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Biological Weapons: A Module for Nursing Professionals
Brucellosis wikipedia , lookup
Onchocerciasis wikipedia , lookup
Sarcocystis wikipedia , lookup
Sexually transmitted infection wikipedia , lookup
Traveler's diarrhea wikipedia , lookup
Typhoid fever wikipedia , lookup
Neonatal infection wikipedia , lookup
Gastroenteritis wikipedia , lookup
Neglected tropical diseases wikipedia , lookup
Hospital-acquired infection wikipedia , lookup
Eradication of infectious diseases wikipedia , lookup
Human cytomegalovirus wikipedia , lookup
Herpes simplex virus wikipedia , lookup
United States biological defense program wikipedia , lookup
Yellow fever wikipedia , lookup
History of biological warfare wikipedia , lookup
Ebola virus disease wikipedia , lookup
Trichinosis wikipedia , lookup
Antiviral drug wikipedia , lookup
Hepatitis C wikipedia , lookup
Tuberculosis wikipedia , lookup
Rocky Mountain spotted fever wikipedia , lookup
African trypanosomiasis wikipedia , lookup
Schistosomiasis wikipedia , lookup
Oesophagostomum wikipedia , lookup
Biological warfare wikipedia , lookup
Hepatitis B wikipedia , lookup
Middle East respiratory syndrome wikipedia , lookup
West Nile fever wikipedia , lookup
Henipavirus wikipedia , lookup
Leptospirosis wikipedia , lookup
Coccidioidomycosis wikipedia , lookup
Marburg virus disease wikipedia , lookup
Lymphocytic choriomeningitis wikipedia , lookup
Biological Weapons: Essential Information on Category C Agents Felissa R. Lashley, RN, PhD, FAAN, FACMG Professor, College of Nursing, and Interim Director, Nursing Center for Bioterrorism and Infectious Disease Preparedness, College of Nursing Rutgers, The State University of New Jersey This module on the use of biological agents as bioweapons covers general material, the classification of biological agents as to their use in bioterrorism and gives the most important information regarding the Category C agents according to the Centers for Disease Control and Prevention (CDC) classification. Separate modules address Category A and Category B agents. This module was supported in part by USDHHS, HRSA Grant No. T01HP01407. OBJECTIVES At the completion of this module, participants will be able to: 1. Identify at least 10 factors that make a biological agent or biological toxin suitable for use as a bioterror agent. 2. List the 3 CDC categories for critical biological agents and why they are so categorized. 3. Identify and list CDC Category C biological agents with potential for use in a bioterrorism attack. 4. Describe signs and symptoms of infection with Category C agents. 5. Discuss isolation precautions for each Category C agent. Using Biological Agents as Bioweapons Biological Agents and Bioterrorism Includes microorganisms, especially certain bacteria and viruses, and biological toxins as botulinum toxin, which act like chemical agents. May be directed at humans, plants, animals, and be a threat to crops, livestock, food products (agroterrorism) during processing, distribution, storage and transportation which could cause illness and also have severe economic consequences such as bovine spongiform encephalopathy, and foot and mouth disease. Biological agents can be used as weapons in: Biocrimes Bioterrorism Biowarfare Biological Agents and Bioterrorism-2 Definition: The North Atlantic Treaty Organization (NATO) defines a biological weapons as "the provision of any infectious agent or toxin by any means of delivery in order to cause harm to humans, animals, or plants." Various definitions for bioterrorism have been given. The following may be used: "the intentional use or threat of use of biological agents on a population to achieve political, social, religious, ethnic, or ideological ends by causing illness, death and wide scale panic and disruption." The aim may not be maximum damage but rather a political statement. Biological Agents and Bioterrorism-3 The technology exists to modify existing biological agents, or weaponize them, to, for example, make it easier to disseminate and/or cause greater harm in their dissemination. The use of biological agents for bioterrorism has been referred to as the "poor man's nuclear bomb." All involve the use of biological agents in order to obtain an outcome: political, social, economic, theological, personal. Agents with Potential for USE in BIOTERRORISM Varies according to source NATO handbook lists 39 agents World Health Organization (WHO) has another list Centers for Disease Control and Prevention (CDC) lists biological agents in various categories, A, B &C National Institute for Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH) also lists categories A, B & C, but they differ somewhat from how CDC categorizes agents and lists a greater number of agents Others The Following are Desirable Characteristics for Biological Agents to be Used for Harmful Intent Generate high levels of panic among population Easy to obtain Inexpensive Easy to produce in mass quantities Can be relatively easily “weaponized” or altered for maximum effect (even with genetic manipulation) High infectivity High person-to-person contagion High mortality The Following are Desirable Characteristics for Biological Agents to be Used for Harmful Intent-2 Lack of effective treatment Need for intensive care, straining resources High potential for casualities/morbidity Result in lengthy illness with prolonged care needed Non-specific symptoms, especially early, delaying recognition Long incubation periods Hard to diagnose Great degree of helplessness from effect Examples of Historical Uses of the Deliberate Release of Biological Agents Known as early as the 6th century BC Soldiers dropped corpses of those who died of plague over city walls during siege of Kaffa to start a plague epidemic and force surrender. British soldiers used variola contaminated blankets to spread smallpox to American Indians during the French and Indian Wars (1754-1767). Examples of Historical Uses of the Deliberate Release of Biological Agents-2 Followers of Bhagwan Shree Rajneesh intentionally contaminated salad bars in The Dalles, Oregon with Salmonella. The purpose was to keep people from voting in a local election in November, 1984. More than 750 people were affected. The Aum Shinrikyo group in Japan attempted to carry out attacks using aerosolized anthrax spores and botulinum toxin before releasing sarin in the Tokyo subway in 1995. Examples of Historical Uses of the Deliberate Release of Biological Agents-3 Intentional distribution of anthrax spores mainly through the US mail to various people occurred in the fall of 2001. In all, there were 22 known cases of anthrax; 11 were inhalational. Pictures from CDC Categories of Critical Biological Agents as Specified by CDC Three Categories of Agents: Category A Agents: Pose the greatest threat to national security Category B Agents: Second highest priority to national security Category C Agents: Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future Category A Agents Pose a threat to national security because they: Can be easily disseminated or transmitted person-to-person Cause high mortality with potential for major public health impact Might cause public panic and social disruption Require special action for public health preparedness Category B Agents Second highest priority to national security: Are moderately easy to disseminate Cause moderate morbidity and low mortality Require specific enhancements of CDC's diagnostic capacity and enhanced disease surveillance Category C Agents Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future because of: Availability Ease of production and dissemination Potential for high morbidity and mortality and major health impact Category C Agents These agents include the following organisms with the disease in parentheses. Each is individually discussed in the following material: Hantaviruses (Hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome Mycobacterium tuberculosis (multidrug-resistant) [MDRTB] Nipah virus (encephalitis) Tickborne encephalitis virus Tickborne hemorrhagic fever viruses Yellow fever virus (yellow fever) Other emerging pathogens such as melioidosis and SARS (not covered here) Source: CDC (2000). Biological and chemical terrorism: Strategic plan for preparedness response. MMWR, 49(RR-04), 1-14. Hantaviruses Description: The genus hantavirus contains many worldwide viruses. Hantaviruses belong to the Bunyavirus family. They are RNA viruses. In humans, infection may result in Hantavirus pulmonary syndrome (HPS) or Hemorrhagic fever with renal syndrome (HFRS) depending on the type of virus. Hantaviruses-2 Epidemiology: The virus types that are known as Old World include such viruses as Puumala, Hantaan, Seoul, Dobrava, and Saaremaa and are found mostly in Europe and Asia. The clinical presentation is that of HFRS. Those known as New World hantaviruses, naturally found in the U.S., and the Americas include the Sin Nombre virus first identified in May 1993 in the U.S. Four Corners area. Infection with Sin Nombre, Andes, bayou, New York and similar hantaviruses can result in HPS. Hantaviruses-3 Transmission: Hantaviruses are transmitted to humans from small mammal carriers that are chronically infected, especially rodents. Most hantaviruses are associated with a particular species of small mammal. The infected rodent sheds virus in feces, saliva and urine. They are transmitted via aerosolization of rodent feces, salive or urine, through the bite of an infected rodent or contamination of broken skin by rodent saliva or excreta, or possibly through ingestion of food or water that are contaminated. Hantaviruses-4 Incubation period: For HFRS, typically 2 to 4 weeks. For HPS, 5 days to 4 weeks, typically 14 to 17 days. Photo from CDC Hantaviruses-5 Clinical manifestations: HFRS – Depends somewhat on which virus causes infection. Infection varies from subclinical to fatal. Typically there is a febrile phase followed by headache and then nausea, vomiting and abdominal pain. Visual disturbances have been noted, particularly a thickening of the lens. Flushing may be seen. Hypotension and shock may develop rapidly. Renal symptoms including back pain and tenderness, may begin at approximately the 3rd or 4th day, and oliguria, anuria and acute renal failure may occur. Hemorrhagic manifestations such as petechiae, hematuria or melena may be seen. A diuretic phase with polyuria may occur with recovery, and full recovery may take weeks. Dobrava infection may be more severe than Puumula infection. Hantaviruses-6 Clinical manifestations cont.: HPS Typically there is a prodromal stage that is characterized by a flu-like illness including fever, chills, malaise and myalgia especially of large muscle groups in legs, shoulders, thighs and lower back. Other symptoms include nausea, vomiting, diarrhea, headache and then cough. May have thrombocytopenia. After this, a cardiopulmonary phase with increasing respiratory and cardiovascular compromise occurs with shortness of breath, tachypnea and tachycardia as well as decline in oxygen saturation and hemoconcentration. Symptoms may resemble adult respiratory distress syndrome. Patients may need mechanical ventilation. In some, milder cases occur. Hantaviruses - Diagnosis HFRS: Diagnosis based on serological and clinical findings. HPS: From characteristic clinical findings, exposure to rodent contaminated areas in history (not useful in bioterrorism), radiological appearance of bilateral diffuse interstitial pulmonary infiltrates but confirmed with serological diagnosis such as Western blot assay or by viral identification in tissues. Hantaviruses & Treatment HFRS: IV ribavirin useful in some cases. Supportive care (see below). HPS: Requires aggressive cardiopulmonary support preferably in intensive care. Patients may need mechanical ventilation, hemodynamic monitoring with a pulmonary artery catheter, supplemental oxygen, appropriate fluid management to maintain cardiac output, and pressors. In the initial care of patients in New Mexico in the early 1990s, extracorporeal membrane oxygenation was useful. Antiviral therapy with ribavirin has been tried with varying reports of success. Hantaviruses cont. Nursing care: Intensive supportive care as discussed above under treatment. Standard isolation precautions. Vaccination: Inactivated vaccines used for old world hantaviruses and in development for others. Other: Although classified as a category C agent, several characteristics make it unlikely for use by terrorists, including difficulty in production and because it is not usually transmitted between humans. Many preventive techniques are available for naturally occurring hantavirus infection not covered here. Sources: Clement, J.P. (2003). Hantavirus. Antiviral Research, 57, 121-127. Lashley, F.R., & Durham, J.D. (Eds.). (2007). Emerging infectious diseases: Trends and Issues,2nd edition . New York: Springer Publishing Co. Lednicky, J.A. (2003). Hantaviruses. Archives of Pathology and Laboratory Medicine, 127, 30-35. Snell, N.J. (2004). Novel and re-emerging respiratory infections. Expert Review in Anti-Infective Therapy, 2, 405-412. Vapalahti, O., Mustonen, J., Lundkvist, A., et al. (2003). Hantavirus infections in Europe. Lancet Infectious Diseases, 3, 653-661. Multidrug-Resistant Tuberculosis (MDR-TB) MDR-TB is considered as a Category-C biological agent by the CDC in regard to its potential for use in bioterrorism. MDR-TB Definition: MDR-TB is defined as a case of TB caused by a strain of M. tuberculosis that is resistant to two or more antituberculosis drugs. Some define MDR-TB as a case of TB caused by a strain of M. tuberculosis that is resistant to isoniazid and rifampin. XDR-TB (extensively resistant tuberculosis) refers to cases of TB that are resistant to isoniazid, rifampin, the second line drugs, the fluoroquinolones, and at least one of three injectable drugs, such as amikacin, kanamycin or capreomycin MDR-TB-2 Etiology: Both tuberculosis infection and tuberculosis (TB) are due to the tubercle bacilli. The most common in the US is Mycobacterium tuberculosis. M. tuberculosis is a nonmotile, non-spore forming rod shaped bacillus with no capsule. It does not produce toxin. It is known as acid fast because of staining characteristics. It can survive for long periods under adverse conditions. MDR-TB-3 Description: Infection with M. tuberculosis can be pulmonary or extrapulmonary. Pulmonary TB is the most common form in developed countries. In extrapulmonary TB, signs and symptoms depend on the affected organ system as well as systemic symptoms. Major concerns about MDR-TB arose in the early 1990s when nosocomial outbreaks occurred. MDR-TB-4 Epidemiology MDR-TB is particularly common in: Resource poor areas Global "hot spots" such as some areas in the former Soviet Union, India, the Dominican Republic, Ivory Coast, and others Congregate settings such as prisons or long-term care facilities MDR-TB Epidemiology cont.-2 In practice, MDR-TB develops either because the person is infected initially with a: Drug-resistant strain (primary), or Susceptible strain that becomes resistant (secondary) Primary resistance would be most likely in regard to bioterrorism use MDR-TB Epidemiology cont.-3 Reasons for secondary resistance are numerous and complex: Wrong drugs used in an improper way Failure to assess drug susceptibility patterns of the organism A large bacterial load, especially in the case of cavitation Poor adherence to the treatment regimen MDR-TB Epidemiology cont.-4 TB (including MDR-TB) and HIV co-infections are relatively common globally and each condition adversely affects the other. In the US in 2007, the overall number of TB cases reported in the U.S. was 13,293 In the U.S. between 1993 and 2006, 49 cases of XDR-TB were reported, and in 2006, 116 cases of MDR-TB were reported. The overall case rate was 4.4 cases per 100,000 population. U.S. born blacks and foreign born persons account for a disproportionate number of cases. MDR-TB Epidemiology cont.-5 TB remains a major global problem. Each year about 2 million people die of TB each year worldwide, and overall one-third of the world’s population is infected. MDR-TB Transmission: Person-to-person through inhalation of droplet nucleii Infected person usually coughs or sneezes and projected infected droplet nucleii into the air Ingestion of contaminated food or water (rare in US) Direct inoculation (rare) although infection through transplant has occurred. MDR-TB Outcomes of Contact with M. tuberculosis Many factors determine outcome such as: Host susceptibility, such as genetic factors and immune status Organism characteristics, such as virulence Environment, such as length of time and proximity of contact between the susceptible person and the person with TB MDR-TB Sequence of Events in Brief: After M. tuberculosis enters the body, possible events include: No infection Tuberculous infection Remains dormant in latent form (90%) Progression to clinical disease (10%) Within a year or two (5%) Years later (5%) MDR-TB Thus, persons may have: Latent TB infection in which they are infected with tubercle bacilli but are not infectious to others nor show clinical symptoms but do usually have a positive reaction to the tuberculin skin test but usually negative chest radiograph. They may be candidates for preventive drug therapy, OR Active TB in which they are infected with tubercle bacilli, usually have positive sputum smears and cultures, usually have a positive reaction to the tuberculin skin test, usually have clinical symptoms, and may be infectious to others before treatment is effective. MDR-TB Clinical Manifestations MDR-TB or XDR-TB are not clinically distinguishable from drug-susceptible TB at the outset. Signs, symptoms and radiological findings are similar initially to drugsusceptible TB. MDR-TB In the non-bioterrorist setting, reasons to suspect drug resistance are: A history of previously treated TB in a person presenting with active TB High community rates of drug resistant TB Positive HIV status High likelihood of exposure to nosocomial, prison or community sources of MDR-TB The infected person is from a country with a high MDR-TB rates Contacts with persons with MDR-TB Infected person has received inadequate treatment regimens for >2 weeks Smears or cultures remain positive despite 2 months of treatment for TB MDR-TB Symptoms of Pulmonary TB include: Cough (usually productive and maybe bloody) Low-grade fever Sweating Chills at night Fatigue Malaise Anorexia Weight loss Dull, aching chest pain or tightness Symptoms of extrapulmonary TB depend on the organ system involved but may include systemic symptoms such as malaise MDR-TB Diagnosis generally consists of: Medical history, Clinical signs and symptoms, Chest x-ray for pulmonary TB, Sputum smear and/or culture for acidfast bacilli, and possibly A tuberculin skin test. MDR-TB Diagnosis Notes Tuberculin skin test with purified protein derivative as screen; anergy may be seen in elderly and the immunosuppressed. Chest x-ray or radiograph of extrapulmonary site shows characteristic findings of abnormalities in apical or posterior segments of upper lobe or superior segments of lower lobe but is not used to confirm diagnosis of pulmonary TB. Appearance may be unusual in HIV-positive persons Sputum smears and cultures for tubercle bacilli. MDR-TB Treatment Initial non-MDR-TB therapy especially in drug-susceptible disease calls for 8 weeks of therapy with isoniazid, rifampin, pyrazinamide, and ethambutol followed by a continuation regimen of isoniazid and rifampin for 18 more weeks as the most frequent option. Aggressive treatment is suggested. MDR-TB Treatment cont. Usually the regimen for MDR-TB will consist of at least 3 TB drugs the patient has not used before (a single drug should never be added) and as many as 6 drugs. There are detailed dosages and possible options available depending on many factors. Newest guidelines should always be consulted MDR-TB Treatment cont. MDR-TB treatment depends on the drug resistance pattern present: It may include directly observed therapy Occasionally, surgical resection may be used in treatment Detailed information about management options are given in the references (see CDC reference in particular) MDR-TB Prevention MDR-TB may be prevented by clinicians: Choosing the appropriate therapeutic regimen based on clinical, microbiological, pathological, radiological and epidemiological information, and Assuring a regimen with the highest likelihood of adherence to therapy. MDR-TB Management, including Infection Control Teaching the patient and family about preventing transmission, especially etiquette and hygiene, use of masks where indicated, and handwashing. Isolation precautions are usually needed until there have been 3 negative sputum cultures. Ascertaining likelihood of adherence and using measures to enhance adherence. Promptly isolate persons suspected or known to have TB. Use appropriate infection control. MDR-TB For sputum positive pulmonary MDR-TB, appropriate infection control includes: Special airborne infection isolation control precautions, including isolation in a negative pressure isolation room. Staff should wear appropriate personal protective devices, and close door behind them. Staff should remove personal protective devices before exiting anteroom and sanitize hands after leaving room. See infection control module details, and CDC, (2005). Guidelines for preventing the transmission of Mycobacterium tuberculosis in health care settings. MDR-TB References CDC. (2003). Treatment of TB. American Thoracic Society, Centers for Disease Control and Prevention, and Infectious Disease Society of America. MMWR, 52 (RR-11), 1-88. CDC (2008). Trends in tuberculosis- United States, 2007. MMWR 57, 281-85. CDC (2005) Guidelines for preventing the transmission of Mycobacterium in healthcare settings, 2005. MMWR, 54, 1-141. Lashley, F. R., & Durham, J. D. (Eds.). (2007). Emerging infectious diseases: Trends and issues. 2nd edition New York: Springer Publishing Co. Mukherjee, J. S., Rich, M. L., Socci, A. R. et al. (2004). Programmes and principles in treatment of multidrug-resistant tuberculosis. Lancet, 363, 474-481. Murphy, R.A. (2008) The emerging crisis of drug-resistant tuberculosis in South Africa: Lessons from New York City. Clinical Infectious Diseases 46, 1729-1732. Yew, W.W. and Leung, C.C. (2008) Management of multidrugresistant tuberculosis: Update 2007. Respirology, 13, 21-46. Nipah Virus Infection CDC Nipah Virus Infection-2 Etiologic agent: Nipah virus, a paramyxovirus Epidemiology: First identified in 1998 after an outbreak of encephalitis in farm and laboratory workers in Malaysia at the same time as illness in pigs. Later spread to Singapore. Bats appear to be the natural host of the virus. Believed that environmental events such as drought and tree cleaning led to bats being closer to pigs, transmitted virus to pigs, then to humans. Nipah Virus Infection-3 Incubation period: Transmission: 4 days to 2 months In most, 2 weeks or less Transmitted between bats, humans, and pigs Humans infected secondarily by droplet transmission Clinical course: Can be similar to subacute sclerosing panencephalitis, caused by the measles virus Infected people can be initially asymptomatic and develop encephalitis months after exposure. May also cause pneumonitis. NIPAH Virus Infection-4 Clinical manifestations may include: Encephalitis with myoclonus Pneumonitis-in some fever, headache Fever Dizziness Headache Vomiting Reduced levels of consciousness Confusion Brain-stem dysfunction Aneflexia Hypotonia Hypertension Tachycardia NIPAH Virus Infection-5 Complications may include: Septicemia GI bleeding Renal impairment Of those recovering, about 1/4 had residual neurological defects Mortality: May approach 40% of those with severe illness NIPAH Virus Infection-6 Treatment: Supportive Ribavirin appears useful Nursing Considerations: Standard isolation precautions Human to human spread not known Supportive and symptomatic nursing management Sources: CDC. Hendra virus disease and Nipah virus encephalitis, October 19, 2007. Solomon, T. (2003). Exotic and emerging viral encephalitis. Current Opinion in Neurology, 16, 411-418. Wong, K.T., Shieh, W.J., Zaki, S.R., et al. (2002). Nipah virus infection, an emerging paramyxoviral zoonosis. Springer Seminars in Immunopathology, 24, 215-228. Tick-Borne Encephalitis Etiology: Tick-borne encephalitis virus (TBEV), a flavivirus Has 3 subtypes: Far Eastern, Siberian, and European TBEV-2 Epidemiology: Endemic to central and eastern Europe, and the far east. Natural habitat is forest undergrowth in Europe and Asia where TBEV is maintained in a cycle involving ticks and animal hosts especially rodents but also larger animals such as goats, cows, and sheep. These ticks need certain climactic conditions that determine their distribution. Global satellite data have contributed to this knowledge. TBEV-3 Transmission: Under natural conditions, most commonly through Bite of infected tick Ingestion of unpasteurized milk Laboratory cases have been acquired through needlestick and through aerosol infection when glass bottles with high TBEV concentrations were accidentally broken. There could be a potential for freeze-dried TBEV to be stored in glass and then broken to allow release of TBEV into the air. A small number of cases from blood transfusion, breast feeding and slaughter of goats have been described. May be excreted in urine and feces. Could cause “significant problems on small scale” if used in bioterrorism. TBEV-4 Incubation period: 7-14 days typically but can be 2 to 28 days. Clinical manifestations: 70-95% of naturally-acquired human infections in endemic areas are subclinical or asymptomatic. Onset is usually abrupt, and early symptoms include fever, fatigue, nausea, vomiting, muscular pain especially in neck, shoulder, lower spine and limbs. TBEV-5 Clinical manifestations cont.: After the initial symptoms, there are various forms of TBE that may develop (discussed in following frames), and a short afebrile period may occur. The Eastern subtype is said to follow a monophasic course. The Western subtype tends to be biphasic. In the febrile form (occurring in about 1/3), no neurological symptoms are seen and recovery is usually complete. TBEV-6 Clinical manifestations cont.: 1. Meningeal form severe headaches, photophobia and pain in the eyes. b. Fever may last 1 to 2 weeks. Recovery is gradual. a. 2. Meningoencephalitis form hallucinations, may become unconscious. b. Can develop bradycardia, gastric hemorrhage, hyperkinesia, hemiparesis, and hemiplegia as well as epileptic seizures. c. Mortality is up to 30%; recovery is slow, and hemiplegia may last. a. TBEV-7 Clinical manifestations cont.: 3. Poliomyelitic form a. Weakness, numbness or paralysis in a limb. b. May have paresis of neck, shoulder and upper limbs, wrist drop and drooping head on standing, muscle atrophy. c. Patients show progressive deterioration, and about half show partial recovery from the neurological manifestations. TBEV-8 Clinical manifestations cont.: 4. Polyradiuculoneuritic form – a. After onset in first phase, temperature returns to normal for 1 to 2 weeks after which symptoms of CNS damage and meningeal and focal neurological symptoms occur. b. There is peripheral nerve pain. c. Recovery is usually complete. 5. Chronic form – a. After the acute disease symptoms, neurological symptoms may develop over a long period even years and can include lateral sclerosis, progressive muscle atrophy and a Parkinson like disease. b. Mental deterioration and dementia may also occur. TBEV-9 Treatment: Supportive, depends on manifestations. Close observation is needed because neuromuscular paralysis leading to rapid respiratory failure may develop quickly, and ventilatory support with intubation may be needed. Nursing Considerations: Use standard precautions for infection control. Supportive depending on manifestations. Close observation is needed because neuromuscular paralysis leading to rapid respiratory failure may develop quickly, and intubation and ventilatory support may be needed. TBEV-10 TBEV Vaccine: Active vaccines are available Other: Postexposure passive immunization with specific immunoglobulin is no longer recommended. Sources: Dumpis, U., Crook, D., & Oksi, J. (1999). Tick-borne encephalitis. Clinical Infectious Diseases, 28, 882-890. Gritsun, T.S., Lashkevich, V.A., & Gould, E.A. (2003). Tick-borne encephalitis. Antiviral Research, 57, 129-146. Lindquist, L, and Vapalahti,O. (2008). Tick-borne encephalitis. Lancet 371, 1861-1871. Tickborne Hemorrhagic Fever Viruses Includes: Omsk hemorrhagic fever virus Kyasanur forest disease virus Both are small, single stranded RNA flaviviruses Diseases caused: Omsk hemorrhagic fever Kyasanur forest disease Tick borne Hemorrhagic Fever Viruses-2 Epidemiology: Both are transmitted through infected ticks. For Kyasanur forest disease virus, the natural host are monkeys, and the region where it is typically found is Northern India. Forest workers are at particular risk. For Omsk hemorrhagic fever virus, the hosts are typically rodents especially muskrats and voles, and the region where it is typically found is Siberia. Incubation period: 2 to 9 days for both Tickborne Hemorrhagic Fever Viruses-3 Clinical manifestations: Omsk hemorrhagic fever Begins with fever, cough, conjunctivitis, maybe hyperemia of face and trunk but no rash There may be papulovesicular eruption in throat, lymphadenopathy, splenomegaly. May see nosebleeds, conjunctival hemorrhaging, gastrointestinal bleeding. May develop pneumonia and/or central nervous system dysfunction. Tickborne Hemorrhagic Fever Viruses-4 Clinical manifestations cont.: Kyasanur Forest disease Similar to Omsk but biphasic appearance of symptoms is common. Begins with sudden onset of fever and headache, backpain, pain in extremities and prostration. Conjunctivitis may be seen and bradycardia may be present. After initial symptoms may see an afebrile period of 9 to 21 days. Up to about half develop meningoencephalitis. On autopsy, see liver and spleen degeneration as well as hemorrhagic pneumonia in some. Tickborne Hemorrhagic Fever Viruses-5 Mortality: Treatment: Up to 10% Supportive Nursing Considerations: Supportive, depending on symptoms. Standard isolation precautions in clinical setting. In laboratory, precautions are taken to protect against airborne droplets, and this may be necessary if widely aerosolized in attack. Tickborne Hemorrhagic Fever Viruses-6 Vaccine: Inactive virus vaccine is available for Kyasanur Forest disease. Other: Handled as biosafety level 4. Sources: Borio, L., Inglesby, T., Peters, C.J., et al. (2002). Hemorrhagic fever viruses as biological weapons. JAMA, 287, 23972405. Kyasanur Forest disease. Traveler's health prevention against diseases abroad. Retrieved July 26, 2008 from: http://www.traveldoctoronline.net/vk_home/index.htm. Gowld, E.A., and Solomon, T. (2008). Pathogenic flaviriviruses. Lancet 371, 500-509. Yellow Fever Etiology: Yellow fever virus, a flavivirus causing viral hemorrhagic fever Epidemiology: Occurs mainly in tropical Africa and South America Has two cycles: Urban pattern of interhuman transmission, with the mosquitos of Aedes aegypti as vectors Sylvatic cycle, involving monkeys and Haemogogus and Sabethes mosquitos Considered a zoonotic infection Yellow Fever-2 Incubation period: 3-6 days usual Clinical manifestations: Clinical disease can range from non-specific to hemorrhagic fever. Person appears acutely ill. Symptoms include: fever, chills, malaise, headache, dizziness, nausea, myalgia, lower back pain, bradycardia, and may have congested conjuctivae. May progress to: prostration, hemorrhage, shock. Yellow Fever-3 Clinical course: Acute illness gives way to apparent remission for about 24 hours; and in some, disease "aborts." In 15-25%, illness reappears and is more severe (period of intoxication). In this phase, may see: Fever Vomiting, may be black Epigastric pain Jaundice and hepatic injury Renal failure Myocardial injury May be major hemorrhagic manifestations, such as epitaxis, melena, hematemesis, ecchymoses Yellow Fever-4 Diagnosis: Detection of virus or viral antigen in blood, serologic diagnosis by measurement of IgM antibodies by ELISA. Complications: Before death, may see: Hypotension Delirium Stupor Coma Metabolic acidosis In those surviving, there is a long convalescent period with weakness and fatigue. There may be tubular necrosis requiring dialysis, as well as pneumonia and hepatic injury. Mortality: 20-50% of patients with hepatorenal disease die. Yellow Fever-5 Treatment: Vaccination: Largely supportive, depending on manifestations. Higerdose ribaviris with interferons may hold promise. Live, attenuated 17D vaccine available Nursing Considerations: Supportive care with standard isolation precautions Sources: Bryant, J., Wang, H., Cabezas, C., et al. (2003). Enzootic transmission of yellow fever virus in Peru. Emerging Infectious Diseases, 9(8), 926-934. Marfin, A.A., Eidex, R.S., Kozarsky, P.E., & Cetron, M.S. (2005). Yellow fever and Japanese encephalitis vaccines: Indications and complications. Infectious Disease Clinics of North America, 19, 151-168. Monath, T.P. (2008). Treatment of Yellow fever: Antiviral Research 78, 116124.