Biological Weapons: Essential Information on Category A Agents

Biological Weapons: Essential Information on Category A 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 A Agents according to the Centers for Disease Control and Prevention (CDC) classification. Separate modules address Category B and Category C agents. This module was supported in part by USDHHS, HRSA Grant No. T01HP01407.

The format and information in this module
focuses on the use of the agent or outbreak of disease particularly in regard to bioterrorism including emphasis on management with nursing applications and infection control material. Detailed material on general transmission of disease, infection control and isolation precautions is in a separate module and this should be consulted. Aspects of preparedness are also in a separate module. Note that for the care of persons exposed to any biological agent, the nurse should be sure he/she is adequately protected first.

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 A biological agents with potential for use in a bioterrorism attack. 4. Describe the signs and symptoms of infection with Category A agents. 5. Discuss isolation precautions for each Category A agent.

Using Biological Agents as Bioweapons

Biological Agents and Bioterrorism
Includes microorganisms, especially certain bacteria and viruses, and biological toxins such 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 and Bioterrorism-2
Biological agents can be used as weapons in: Biocrimes Bioterrorism Biowarfare Definition: North Atlantic Treaty Organization (NATO) defines a biological weapon 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.

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 CDC lists biological agents in various categories, A, B, and C National Institute for Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH) also lists categories A, B, and 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 casualties/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 ( ).

Examples of Historical Uses of the Deliberate Release of Biological Agents-2
Followers of Bhagwan Shree Rajneesh intentionally contaminated salad bars in the The Dalles, Oregon with Salmonella. The purpose was to keep people from voting in a local election in November, 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 In all, there were 22 known cases of anthrax; 11 were inhalational. Picture from CDC. Inhalational anthrax.

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 A Agents These agents include the following diseases, with the organism in parentheses. Discussion of each individual organism listed below follows: Anthrax (Bacillus anthracis) Botulism (Clostridium botulinum) Ebola hemorrhagic fever (Ebola virus) Lassa Fever (Lassa virus) Marburg hemorrhagic fever (Marburg virus) Plague (Yersinia pestis) Smallpox (Variola virus) Tularemia (Francisella tularensis)

Category A Agents-2 Other hemorrhagic fever viruses, such as:
Junin virus (Argentine hemorrhagic fever) Guanarito virus (Venezuelan hemorrhagic fever) Machupo virus (Bolivian hemorrhagic fever) Sabia virus (Brazilian hemorrhagic fever)

Anthrax (Bacillus anthracis)
Etiology: A gram-positive rod-like bacteria, B. anthracis Capable of aerobic spore formation Spores can last 40 years or more Non-motile Forms capsule

Anthrax-2 Description – has several clinical types: Other names –
Cutaneous (skin) anthrax most common. Gastrointestinal (GI) anthrax Rare in developed countries Results from infected meat that is undercooked or raw Can affect oropharynx or esophagus, causing ulcers Inhalational (respiratory) anthrax Abrupt respiratory distress No person-to-person transmission Other names – Was known as woolsorters or ragpickers disease.

Anthrax-3 Epidemiology:
A zoonotic disease, primarily of animals such as cattle, sheep, goats, deer and horses. Worldwide there can be up to 100,000 cases per year. Most natural cases occur in the Middle East, India, Asia, Africa and Latin America. Usually rare in the US and western Europe. Until the deliberate release of anthrax spores in the US in 2001, inhalational anthrax had not been reported in the US for more than 20 years. In 2001, 22 cases of human anthrax were reported in the US, 2 in 2002, none in 2003, 2004, and 2005, 1 in 2006, and none in 2007.

Anthrax-4 Transmission:
Animals become infected through ingestion of spores in soil which germinate and produce toxins. Humans usually contract anthrax from contact with anthrax infected animals or contaminated animal hair, hides, flax, wool, excretions, blood and products such as bone meal. Direct contact from infected person’s skin lesions. Inhalational anthrax is acquired by inhaling aerosolized spores. Gastrointestinal anthrax results from eating undercooked or raw meat or dairy products from infected animals. Inhalational and gastrointestinal anthrax are not known to be transmitted person-to-person. Humans may also become infected through intentional exposure.

Anthrax-5 Transmission cont.:
Occupational exposure in humans has been the most usual way in which anthrax was acquired. Examples include farm workers, laboratory workers or industrial exposure (see below). Cutaneous and inhalational anthrax cases formerly occurred during the manufacturing process of infected wool, hair and hides. In 2006, one case occurred in a man who acquired the disease from an infected animal hide he brought back from Africa to make drums.

Anthrax-6 Incubation period: Cutaneous anthrax: a few hours to 12 days
Gastrointestinal anthrax: 1 to 7 days Inhalational anthrax: Less than 7 days (usually 4-6 days) but up to 2 months.

Anthrax-7 Clinical manifestations: Cutaneous anthrax
Local response is itching followed by small red macule progressing to papule formation (3-5 days usual), resembling an insect bite. This becomes a vesicle with a painless ulcer formation that may enlarge to 1 to 3 cm. Black eschar develops within 7-10 days with surrounding edema. Typically seen on arms, hands, head or neck. May also have lymphadenitis and fever, malaise and headache. Septicemia can occur.

Cutaneous Anthrax (Notice the edema and typical lesions) Photos from CDC.

Further examples of Cutaneous Anthrax lesions Photos from CDC.
Black eschar, redness remains Ulcer and vesicle ring

Anthrax-8 Clinical manifestations cont.: Gastrointestinal anthrax
Symptoms initially are nausea, vomiting, anorexia, fever, followed by abdominal pain, hematemesis and bloody diarrhea. Symptoms depend on site of lesions. If there are lesions in oral pharynx, may swell to affect the airway, and there may be dysphagia and throat pain. In gastrointestinal anthrax, ascites may develop as may septicemia within 5 days after onset.

Anthrax-9 Clinical manifestations cont.: Inhalational anthrax
There are usually two phases. Initial symptoms are nonspecific and consist of malaise, low grade fever, nonproductive cough and gastrointestinal complaints such as nausea and/or vomiting. Sometimes there is improvement for a few days followed by a second phase with dry cough, dyspnea, high fever, chills, diaphoresis, tachypnea and respiratory distress. Bacteria enter the blood causing bacteremia, and seeding of the meninges and gastrointestinal tract. Abdominal pain, hematemesis, melena, cyanosis, confusion and hemorrhagic, purulent meningitis develop.

Anthrax-10 Clinical manifestations cont.: Inhalational anthrax cont. –
Meningitis occurs in about 50%. Cardiovascular collapse and death follow if untreated. Because early symptoms are non-specific, the presence of nausea and vomiting and neurological symptoms help to differentiate it from other disorders and a widened mediastinum on x-ray is suggestive of inhalational anthrax.

Inhalational Anthrax Mediastinal widening and pleural effusion on Chest X-Ray in inhalational anthrax

Anthrax-11 Diagnosis: For all, blood cultures may be done if organism has spread. Lab may do rapid screening followed by confirmatory testing. Combine lab testing with clinical findings.

Anthrax-12 Diagnosis cont.: Cutaneous – Gastrointestinal –
Gram stain, PCR, culture of exudate or eschar Should be done before antibiotic therapy Gastrointestinal – Blood cultures Oropharyngeal swabs Inhalational – Chest x-ray findings especially widened mediastinum, pleural effusions, and pulmonary congestion Tissue biopsy Fluid for gram stain, PCR or culture if from sterile site

Anthrax-13 Mortality: Cutaneous - if untreated can be 10%-20%, less than 1% with treatment Gastrointestinal - depends on site, 25%-60% Inhalation - mortality can be 45%-97% with antibiotic therapy. The case fatality rate may be as high as 75%.

Anthrax-14 Treatment: Cutaneous anthrax – Inhalational anthrax –
Initial therapy in adults is usually ciprofloxacin or doxycycline; in children both are also used, although care must be taken in children as doxycycline may discolor teeth. Therapy may be oral. Inhalational anthrax – For adults and children, ciprofloxacin or doxycycline are used with one or two additional antimicrobials. Initial therapy is IV, switching to oral therapy when appropriate. Therapy may be as long as 60 days. Therapy may be combined with a 3 dose regimen of anthrax vaccine for prophylaxis.

Anthrax-15 Treatment cont.: Gastrointestinal anthrax –
May be treated with the same antibiotic regimens as inhalation because of potential to spread to respiratory tract. Note: Post-exposure prophylaxis may be given to those exposed to an initial release of anthrax as soon as possible after exposure. This is usually administered orally for 60 days with ciprofloxacin and doxycycline being the most desired followed by amoxicillin which is preferred for pregnant women. If organism is susceptible, children may also be switched to amoxicillin.

Anthrax-16 Nursing considerations:
Be sure decontamination has taken place. Appropriate isolation precautions. Supportive care as needed for symptoms. If associated with intentional release, psychosocial support/therapy is needed. In analysis of survivors of fall 2001 anthrax release, a year later survivors had reported lower health-related quality of life and greater overall psychological distress. Those who had inhalation anthrax reported loss of functional capacity, and some still had respiratory abnormalities. Adherence may be an issue for persons on long-term antimicrobial therapy and nurses should plan to address this.

Anthrax-17 Isolation Precautions:
Cutaneous anthrax – Standard and the transmission based contact precautions. Avoid any contact with skin lesions or drainage. Inhalational anthrax – Both standard and contact precautions have been recommended in addition to respurology N95 mask or PAPR & protective clothing for environmental aerolized powder on person. Gastrointestinal anthrax – Standard precautions.

Anthrax-18 Vaccine: Other:
Multidose vaccine available but currently used for special populations such as the military. Both live cellular and live acellular vaccines are available. Recombinant vaccines are in development. Other: Persons known to be exposed to anthrax spores should remove clothing and shoes and leave at worksite and wash exposed skin including any jewelry and glasses. Removed clothing should be bagged. At home, systematic showering with systematic cleaning from hair down should be done if at risk for higher contamination. Care needs to be taken when removing outer clothing to keep inner clothing from being contaminated. Biosafety level 2 handling.

Anthrax – Special Considerations Re: Bioterrorism
Anthrax is considered one of the most important biological agents with potential for use as a bioterror agent. It can be weaponized in an aerosolized stable spore form. One deep breath at the site of intentional release can result in inhalational anthrax with high mortality. Environmental surveillance and assessment is needed. Decontamination procedures are needed.

Anthrax – Special Considerations Re: Bioterrorism-2
Anthrax potential for use as bioterror agent cont.: Pre-exposure immunization available for defined population segments. If anthrax is suspected, one part of the patient assessment is to assess whether there is an epidemiological linkage to a plausible environmental exposure such as through the person’s occupation. Antimicrobial prophylaxis will be used for persons potentially exposed to anthrax. In those who are demonstrated not to be exposed, prophylaxis can be discontinued. For others, this will be continued for about 60 days.

Botulism (Clostridium botulinum toxin)
Etiology: Toxin from Clostridium botulism, a spore- forming bacillus. Seven known types cause disease. These toxins are potent neurotoxins. Toxin prevents acetylcholine release and blocks neuromuscular transmission, presynaptic inhibition affecting autonomic and motor receptors. Minute quantities of botulinum toxins can cause death, as they are extremely poisonous. Infective dose: micrograms.

Botulism-2 Types: Foodborne – most common Wound Infant Inhalational - rare, may be intentional Incubation period: For foodborne botulism: hours usual but can be 6 hours to 10 days. Incubation period for inhalation botulism is hours after exposure.

Botulism-3 Epidemiology:
Most cases of foodborne botulism occur through improperly canned or prepared foods especially those that are of low acidity such as corn, beans, tomato sauce. Improperly heated and stored sauteed onions were the cause of one outbreak in Peoria, Illinois. Botulinum toxins have been weaponized to be delivered by aerosol means. Wound and infant botulism are not discussed here.

Botulism-4 Transmission:
Ingestion, inhalation (in deliberate release situation) or absorption. Not transmissable from person-to- person.

Botulism-5 Clinical manifestations: Blurred vision Dilated pupils
Diplopia Ptosis Dry mouth, and Photophobia These may be followed by: Dysarthria Dysphagia Dysphonia Generalized weakness, and A symmetrical descending progressive paralysis leading to respiratory failure.

Botulism-6 Clinical manifestations cont.:
Cranial nerve palsies are responsible for symptoms, such as difficulty in speaking or swallowing. Symptoms such as constipation and urinary retention may be seen and nausea and vomiting may be present. Patients are usually alert and afebrile.

Botulism-7 Diagnosis: By detection of toxin in serum, stools or gastric secretions.

Botulism-8 Treatment: Important to recognize botulism early and administer botulism antitoxin as soon as possible to neutralize the circulating toxin or progression will continue to occur. Antitoxin does not reverse paralysis but limits it. In cases of aerosol exposure, the antitoxin is effective before clinical symptoms are present but if given later will not prevent respiratory failure.

Botulism-9 Treatment cont.:
Full recovery can take a long time—months--as presynaptic axons regenerate and new synapses are formed. In the botulism outbreak in Peoria in the 1980s, symptoms such as fatigue, headache, and weakness lasted for years. Therapy includes rapid administration of botulism antitoxin, monitoring of vital capacity to institute rapid ventilatory support when vital capacity falls below 12 ml/kg.

Botulism-10 Nursing considerations: Use of standard precautions
Isolation room not required Observe for possible respiratory distress which can occur rapidly Assist patient with communication if on a mechanical ventilator Prevent nosocomial infections through use of good hygiene Prevent deep vein thromboses (DVT) Give appropriate bowel and bladder care

Botulism-11 Nursing considerations cont.:
May need extensive rehabilitation for swallowing, speech, muscle strength and so on. Address psychosocial issues and fears associated with the progressive paralysis and loss of voluntary movement and speech. CDC recommends decontamination of patients and their clothing with soap and water if exposed to aerosolized botulism toxins and decontamination of exposed surfaces by cleaning with a bleach solution.

Botulism-12 Other: Prevention:
In case of use in bioterrorism, resources such as ventilatory support (which may be needed in the long term) and supportive intensive care services would be overwhelmed, as would the availability of antitoxin. Prevention: Pre-exposure vaccination with toxoid is available for military personnel and laboratory workers at high risk of exposure. Development of recombinant toxoid vaccines for wider use is underway.

Ebola Hemorrhagic Fever (Ebola virus)
Etiology: Ebola virus, a rod-shaped RNA virus in the filovirus family. Changes shape rapidly. The filamentous form is associated with high infectivity. Has 4 (possibly 5 ) subtypes to date: Zaire Sudan Reston Cote d’Ivoire (Ivory Coast) A possible new subtype responsible for the outbreak in Uganda in Picture from CDC

Ebola-2 Description: Epidemiology:
Is a viral hemorrhagic fever caused by the Ebola virus. Epidemiology: Ebola virus occurs naturally in Africa. While subclinical infections have been noted, typically Ebola hemorrhagic fever emerges in sporadic outbreaks. Outbreaks have been reported in the Democratic Republic of the Congo, Gabon, Sudan, the Ivory Coast, Uganda and Republic of the Congo.

Ebola-3 Epidemiology cont.:
First outbreaks recognized in 1976 in Sudan and in Zaire, now part of the Democratic Republic of the Congo. It is believed to be a zoonotic virus normally maintained by a natural host native to Africa. Photo from CDC.

Ebola-4 Epidemiology cont.:
The natural reservoir for Ebola virus is not known, but it is believed that human outbreaks occur when a person is exposed to an infected animal. Fruit bats have been suggested as having a role. Outbreaks also occur among gorillas and chimpanzees. Ebola-Reston occurred in infected monkeys in the Phillipines, but is not known if Ebola is also native to Asia since there have not been other recognized outbreaks there. The most recent reported outbreaks are in The Democratic Republic of the Congo (2007) and Uganda ( ) The outbreak in Uganda is believed due to a previously unknown subtype with a lower mortality rate.

Ebola-5 Transmission: Person-to-person spread may occur when a person comes into contact with infected blood, tissues, secretions, or excretions of another person. Infection may also occur through contact with contaminated objects. Infection may further occur in hospitals or health care settings through: The use of contaminated medical equipment, such as reused needles and syringes, Contaminated multivials of medicine, and/or Lack of appropriate infection control. Traditional burial ceremonies involving contact with the infected corpse may spread Ebola virus. Handling of infected wild animal carcasses, such as chimpanzees, gorillas and duikers, including food preparation activities.

Ebola-6 Incubation period: 2 to 21 days. Clinical manifestations:
Asymptomatic infection may occur. In most cases, the onset of illness is abrupt with fever, headache, myalgia, weakness, malaise and pharyngitis. These may be followed by nausea, diarrhea and vomiting as well as stomach pain. A maculopapular rash may appear around the 5th day and desquamation can occur. Conjunctival injection, hiccups, and hemorrhage from orifices as well as petechiae and ecchymoses may be seen. Blindness can occur. Obtunding may occur.

Ebola-7 Diagnosis: Mortality:
By antigen-capture enzyme-linked immunosorbent assay (ELISA), IgM ELISA, polymerase chain reaction (PCR), and virus isolation. Mortality: The mortality rate is high, usually 25% to 90%.

Ebola-8 Treatment: Nursing considerations: Supportive
This may include maintenance of appropriate fluid and electrolytes, oxygenation and blood pressure, and treating complications promptly. Immune plasma from convalescent patients has been used in some instances. Nursing considerations: Limit number of staff approaching patient, use mask, gown, gloves, goggles, leg coverings, and shoe coverings. Be sure health care staff understands the infection control procedures in use. Prevent other cases by preventing nosocomial transmission, including to health care staff.

Ebola-9 Nursing considerations cont.:
Appropriate infection control critical. Should use immediate isolation of suspected case with airborne and contact precautions, as well as standard precautions and barrier nursing. Because of the severity of the disease, many practitioners in the field use double masks, gowns, gloves and so on in implementing precautions. Individual room with negative air pressure. In places where no negative pressure isolation rooms exist, the patient should be put in a private room with a HEPA filtration unit. Limit unnecessary blood draws and other procedures. Use N95 or higher respirators for aerosol generating procedures in settings where AIIRs are unavailable.

The patient should remain in their room with doors and windows closed. In full service hospitals, an anteroom may be used between the private room and the corridor. If there are a large number of patients needing care, a designated nursing unit may be created with a barrier plan to seal off the existing ventilation system from other hospital areas and limiting access to the unit. In cases of mass numbers, a whole facility or large gym may be dedicated. Prevent cases through education of family and community about methods of spread and how to avoid them and why these precautions are necessary.

Be sure staff fully understand isolation precautions. During some Ebola outbreaks, governments outlawed traditional ways of preparation of bodies and other burial practices. Specific guidelines are available online for infection control for viral hemorrhagic fever in the African health care setting at: Supportive care depending on manifestations including maintaining appropriate fluid and electrolytes.

Ebola-12 Vaccine: Experimental vaccine in animals

Ebola-13 Prevention: Prevent other cases by preventing nosocomial transmission including to health care staff. Prevent cases through education of the family and community about methods of spread and how to avoid them. The latter should include information that Ebola virus may be transmitted in semen up to 12 weeks after infection.

Ebola-14 Social, behavioral and cultural issues:
Affected families may be stigmatized and not be allowed in other dwellings or schools. Families tend not to seek medical care because of: Cost, Mistrust of hospitals (nosocomial spread supports these fears), Belief in traditional remedies and healers, and Problems of transportation to health care facilities especially in rainy season. Traditional burial practices contribute to person-to-person spread. Civil unrest and wars can exacerbate outbreaks through overcrowding, poor sanitation, and economic dispair.

Ebola-15 Other notes: Ebola outbreaks tend to burn out relatively quickly because of the high mortality rates. Ebola virus is studied in a level 4 biosafety facility. There are great fears that the Ebola virus could mutate into a form that is more easily transmitted from human-to- human or becomes airborne.

Lassa Fever (Lassa virus)
Etiology: Lassa virus, a single stranded RNA virus in the arenavirus family. Description: Is a viral hemorrhagic fever caused by the Lassa virus. Lassa virus electron micrograph. Image courtesy, C.S. Goldsmith and M. Bowen (CDC).

Lassa Fever-2 Epidemiology:
Endemic in West Africa, where it kills thousands per year, especially in Sierra Leone. Fewer cases are seen in Nigeria, Guinea and Liberia. Subclinical infection commonly occurs in areas of rural West Africa where Lassa virus is endemic. This is known through the high prevalence of antibodies to Lassa virus in the serum in seropositivity studies in West Africa. Occasional outbreaks occur, often with high mortality rates. In 2004, a case was identified in a New Jersey man who had recently returned to the Trenton area from Africa, and in 2006 a case was diagnosed in a man who returned to Germany from Sierra Leone.

Lassa Fever-3 Epidemiology cont:
The natural hosts are rodents of the Mastomys genus. These rodents prefer to live in or around human dwellings. These rodents are persistently infected and shed virus in excreta.

Lassa Fever-4 Transmission: Infection results through:
Direct contact with infected rodent urine or droppings, Through touching objects or eating food contaminated by infected excreta, Through breaks in the skin, Through inhalation of infected rodent excreta in aerosol form, such as when cleaning a heavily contaminated area, and Through food preparation or consumption of infected rodents. These rodents are considered a delicacy in this part of Africa.

Lassa Fever-5 Transmission cont.:
Richmond & Baglole (2003) note that Lassa viral antibodies occur after a febrile illness in twice as many people who eat these rodents than in those who do not, and deafness (one of the sequelae of Lassa fever) occurs four times more frequently. Person-to-person spread may occur when a person comes into contact with: Infected blood, Tissues, Secretions, or Excretions.

Lassa Fever-6 Transmission cont.:
Lassa virus is found in semen up to 3 months after infection and in urine a month after disease onset. Infection may also occur in hospitals or health care settings through use of contaminated medical equipment such as needles and syringes that may be reused or through overcrowding and poor hygiene. Traditional burial ceremonies involving contact with the infected corpse may spread Lassa virus (see cultural considerations under Ebola).

Lassa Fever-7 Transmission cont.: Incubation period: 5 to 21 days.
Lassa virus may be excreted in urine up to 9 weeks after infection, and excreted in semen up to 3 months after infection. Incubation period: 5 to 21 days. Clinical manifestations: In about 80%, affected persons are asymptomatic or mildly affected. In 20%, symptoms may be severe and may mimic other hemorrhagic fevers.

Lassa Fever-8 Clinical manifestations cont.:
Richmond & Baglole (2003) divide clinical stages and symptoms as follows: Stage 1 (days 1-3) Symptoms include general weakness and malaise, high fever, about 39o C with higher peaks. Stage 2 (days 4-7) Symptoms include sore throat (with white exudative patches); headache; back, chest, side, or abdominal pain; conjunctivitis; nausea and vomiting; diarrhea; productive cough; proteinuria; low blood pressure (systolic <100 mm/Hg); and anemia. Stage 3 (after 7 days) Symptoms include facial edema; convulsions; mucosal bleeding (mouth, nose, eyes); internal bleeding; and confusion or disorientation. Stage 4 (after 14 days) Symptoms include coma and death. Not all progress through all stages.

Lassa Fever-9 Diagnosis:
Reverse transcription polymerase chain reaction (PCR) can diagnose close to 100% but takes time. Enzyme linked immunosorbent assays (ELISA) for Lassa virus antigen and for virus IgM are more than 85% sensitive and specific together. If laboratory tests are not available, clinical diagnosis should be suspected in patient with fever at or above 38o C or 100.4o F who do not respond adequately to antibiotics or antimalarial drugs.

Lassa Fever-10 Complications: Treatment:
Includes mucosal bleeding, sensorineural deafness, hair loss, loss of coordination, spontaneous abortion in women, and both pleural and pericardial effusion Treatment: Supportive such as fluid replacement. Intravenous ribavirin is effective especially when given early. Thus, early diagnosis and clinical suspicion is needed.

Lassa Fever-11 Management:
Strict standard, contact and droplet isolation of suspected cases and maintaining procedures for handling body fluids and excreta as well as appropriate infection control procedures. Stringent barrier nursing procedures. Limit number of staff approaching patient. Use N95 or higher respirators when performing aerosol – generating procedures.

Lassa Fever-12 Management cont.:
Use mask, face shield, gown, gloves, leg coverings, and shoe coverings. Be sure health care staff understands the infection control procedures in use. Consult

Lassa Fever-13 Management cont.:
Nurses should provide education to patients and families regarding why these precautions and procedures are necessary and how to prevent the spread of the virus. Specific guidelines are available online for infection control for viral hemorrhagic fevers in the African health care setting at:

Lassa Fever-14 Prevention: Vaccination: Experimental Mortality:
Prevent other cases by preventing nosocomial transmission including to health care staff. Prevent cases through education of the family and community about methods of spread and how to avoid them. Vaccination: Experimental Mortality: Varies. In general population may be 1 to 2%, but in those who are hospitalized, is generally estimated at up to 25%. In Sierra Leone, one study indicated that 25% of all maternal deaths were due to Lassa fever (Price, Fisher-Hoch, Craven & McCormick, 1988).

Lassa Fever-15 Social, behavioral and cultural issues:
Because Lassa virus is spread through rodents, families may wish to continue to eat the “sweet meat” of this rodent and not associate that practice with developing Lassa fever since in many cases, infection will be asymptomatic or mild. Affected families may be stigmatized and not be allowed in other dwellings or schools.

Lassa Fever-16 Social, behavioral and cultural issues cont.:
Families tend not to seek medical care because of: Cost, Mistrust of hospitals (nosocomial spread supports these fears), Belief in traditional remedies and healers, Non-availability of a quick early diagnostic test in the field, Problems of transportation to health care facilities especially in rainy season, and Attribution of some complications, such as miscarriage, to “witchcraft” or fault of the woman.

Lassa Fever-17 Social, behavioral and cultural issues cont.:
Traditional burial practices contribute to person-to-person spread. The resulting deafness in some may lead to social isolation. Civil unrest and wars can exacerbate outbreaks through overcrowding, poor sanitation, and economic dispair.

Lassa Fever-18 Other notes:
Lassa fever has been diagnosed in travelers including relief workers and UN peacekeepers returning from West Africa to Europe and North America. A case was imported to New Jersey in August The patient was hospitalized and subsequently died. No further transmission was identified. Lassa fever is studied in a level 3 biosafety facility.

Marburg Hemorrhagic Fever (Marburg virus)
Etiology: Marburg virus, a RNA virus in the filovirus family, the only other member of which is Ebola virus. Description: Is a viral hemorrhagic fever caused by the Marburg virus. Also called Marburg disease. Image courtesy of Russell Regnery, Ph.D., DVRD, NCID, CDC.

Marburg hemorrhagic fever-2
Epidemiology: Marburg hemorrhagic fever was first recognized in 1967 among workers in laboratories in Germany and was then Yugoslavia. The source of this infection was infected green monkeys imported from Africa, specifically Uganda. The next reported index case was in 1975 in a tourist who apparently acquired the infection in Zimbabwe, and who was hospitalized in South Africa. He transmitted Marburg virus to his travel companion and to a nurse who cared for him.

Epidemiology cont.: In 1998, an outbreak occurred in the Democratic Republic of the Congo, and the index case was believed to have acquired infection from a source in a gold mine there. In late 2004 and 2005, an outbreak occurred in Angola. Of the 175 identified cases as of 4/4/05, 155 had been fatal. Other outbreaks were relatively small. Another small outbreak occurred in a mining community in Uganda in In July 2008 a Dutch tourist returned to the Netherlands with Marburg fever. The natural host for Marburg virus is unknown.

Transmission: Person-to-person spread may occur when a person comes into contact with infected blood, tissues, secretions, or excretions, or has close contact with an infected person. Infection may also occur through contact with contaminated objects or through droplets of body fluids. The virus is still found in seminal fluid months after infection, and sexual transmission from a male to a female has been documented.

Incubation period: Typically 3-10 days Clinical manifestations: In most cases, the onset of illness is abrupt with fever, chills, headache, and myalgia. Nausea, vomiting, chest pain, pharyngitis, abdominal pain and severe diarrhea may be seen. A maculopapular rash may appear around the 5th day.

Clinical manifestations cont.: Other severe symptoms such as jaundice; pancreatitis; severe weight loss; delirium; shock; liver failure; massive hemorrhage through vomitus, eyes, skin, and vagina; and multiorgan dysfunction may be seen. Recovery is prolonged and may include hepatitis, transverse myelitis, uvietis, and/or orchitis in men as well as prolonged hepatitis.

Diagnosis: By antigen-capture enzyme-linked immunosorbent assay (ELISA), IgM capture ELISA, polymerase chain reaction (PCR), and virus isolation. Diagnosis can be difficult because signs and symptoms can be similar to diseases such as malaria or typhoid fever or be nonspecific, especially initially. Diagnosis is particularly difficult when only one or a few cases appear.

Treatment: Supportive, and may include: Maintenance of appropriate fluid and electrolytes, Oxygenation, Frequent blood pressure checks, Replacement of lost blood and clotting factors, and Treating complications promptly. Immune plasma from convalescent patients has been used in some instances.

Management: Strict isolation of suspected cases and maintaining procedures for handling body fluids and excreta as well as appropriate infection control procedures using standard, contact, and airborne or droplet precautions. Stringent barrier nursing procedures. Do not wear jewelry. Limit number of staff approaching patient.

Management cont.: Use mask, fluid-proof long-sleeved gown, gloves, goggles, leg coverings and shoe coverings that are at least ankle high and fluid proof (may need to be higher if floor is visibly soiled). Use double disposable gloves if handling any sharp device, and be sure gloves cover cuff of gown. Use hair covering and disposable face shields if needed.

Management cont.: Disposable N-95 respirators should be worn when entering room. Remove shoe covers and gloves as well as gowns before exiting. Wash hands immediately on leaving room with antimicrobial agent. Use disposable equipment when possible or dedicated equipment such as stethoscopes to be kept in patient’s room.

Management cont.: Be sure health care staff understands the infection control procedures in use. Prevent other cases by preventing nosocomial transmission including to health care staff. Specific guidelines are available online for infection control in the African health care setting at Also see information in module discussing infection control, and at

Prevention: Prevent other cases by preventing nosocomial transmission including to health care staff. Prevent cases through education of the family and community about methods of spread and how to avoid them. Should include information that Marburg virus may be transmitted in semen as long as 3 months after infection.

Mortality: The mortality rate is high, usually 23 to 25% or more. Vaccine: Experimental vaccine is being looked at in animals. Other notes: Marburg virus is studied in a level 4 biosafety facility. Knowledge of Marburg hemorrhagic fever and Marburg virus is somewhat limited due to the few number of cases known.

Plague (Yersinia pestis)
Plague is considered a Category A agent for bioterrorism because: Plague bacteria are not difficult to obtain, Aerosolized plague bacteria are easily transmitted, There is a high attack rate, Clinical disease is severe, and The word “plague” has a high psychological impact. A sudden outbreak of disease due to an intentional release might present as severe pneumonia and sepsis.

Plague-2 Picture from CDC

Plague-3 Etiology: Description:
Yersinia pestis, a small gram-negative rod-like bacilli. Description: Was known as the Black death in the bubonic form in the middle ages when it killed million in Europe. In the mid 1800s, it killed 12 million in China.

Plague-4 Epidemiology: Plague is considered a zoonosis.
Y. pestis is transmitted from infected rodents such as rats, mice, gerbils, chipmunks, and prairie dogs to humans via infected fleas. Picture from CDC

Plague-5 Epidemiology cont.:
Cats and dogs, also may become infected by eating infected rodents. Plague occurs worldwide. In the US there are generally 10 to 15 reported cases of plague each year, most commonly in rural areas of New Mexico, Colorado, Arizona, California, Oregon and Nevada. Worldwide there are 1,000-3,000 cases reported each year.

Plague-6 Epidemiology cont.:
In the fall of 2002, a hospital in New York City admitted a couple who were found to have plague acquired in their home state of New Mexico before traveling to New York. Most cases occur in summer. About 30% of cases occur in southwestern US. Suspicion should be raised if it occurs in other geographic areas.

Plague-7 Clinical types:
Bubonic – infected lymph nodes leading to development of buboes. Most common. Septicemic – organisms are blood-borne, primary through dried inoculation or secondary from bubonic or pneumonic plague. Pneumonic – is transmissible by aerosol. Rarest, high mortality.

Plague-8 Transmission: Incubation period: Via bite of infected fleas,
Through contact with infected animals or their fluids, and In pneumonic plague, animal-to-person, or person-to-person via droplets. In bioterrorism, organisms would most likely be transmitted through aerosol dispersion. Incubation period: Bubonic – 2 to 8 days after exposure Pneumonic – 1 to 4 days after exposure

Plague-9 Clinical manifestations:
Y. pestis produces an endotoxin that can lead to shock, sepsis, disseminated intravascular coagulation (DIC), and multiorgan failure. Bubonic – May experience abrupt onset of flu-like symptoms such as fever, chills, headache, and malaise shortly before or at the same time as the bubo which is a swollen, warm, reddened (often around the edges), very tender lymph node(s) usually in the inguinal, axillary or cervical region.

Plague-10 Clinical manifestations cont.: Bubonic cont. –
Patients may become prostrated with episodes of agitation and restlessness. Secondary septicemia may result and this can lead to secondary pneumonic plague. Picture from CDC

Plague-11 Clinical manifestations cont.: Pneumonic (primary) –
Presentation is severe, fulminant, rapidly progressing pneumonia. Signs and symptoms include fever, dyspnea, and cough with hemoptysis, and chest pain. May also have nausea, vomiting, diarrhea, purpura, and abdominal pain.

Plague-12 Clinical manifestations cont.: Septicemic (primary) –
Presentation resembles other gram-negative septicemias including high fever, chills, malaise, hypotension, nausea, vomiting and diarrhea. May also have purpura and disseminated intravascular coagulation (DIC). May spread rapidly to central nervous system resulting in meningitis, lungs and other sites.

Plague-13 Diagnosis: There are three levels of laboratory test criteria for diagnosis according to CDC: Suspected Presumptive Confirmed

Plague-14 Diagnosis cont.:
Diagnosis is by compatibility of clinical symptoms: Along with stain or smear positive specifically for Y. pestis, or if a single serum specimen is tested and the anti-F-1 titer by agglutination is greater than 1:10 (presumptive), Or a small gram-negative coccobacilli from affected tissue (suspected), or if an isolated culture is lysed by specific bacteriophage, If two serum specimens demonstrate a four-fold anti-F-1 antigen titer difference by agglutination testing, or if a single serum specimen tested by agglutination has a titer of more than 1:128, and the patient has no previous history of plague exposure or vaccination history (confirmed).

Plague-15 Mortality: Bubonic – Untreated bubonic plague has a mortality of 40 to 60% but with treatment is less than 10%. Pneumonic – Untreated pneumonic plague has a mortality rate of 95% to 100%. With treatment the mortality rate may still approach 60%. It is essential that antimicrobial treatment begin within 24 hours. Septicemic – Untreated septicemic plague has a mortality rate of essentially 100%. With treatment the mortality rate may still approach 60%. It is essential that antimicrobial therapy begin within 24 hours.

Plague-16 Treatment: Streptomycin, IM every 12 hours has been the therapy of choice followed by gentamicin (5 mg/kg per day) which is more readily available in the US. Doxycycline and the fluoroquinolones are considered alternate therapies. Supportive care, including hemodynamic monitoring, especially for septic shock is necessary. Buboes are generally not incised and drained, but regress with antibiotic treatment. Chloramphenicol may be used for treatment of plague meningitis if it occurs.

Plague-17 Prophylaxis and Vaccination
Post-exposure prophylaxis with doxycycline or ciprofloxacin may be used for those with known exposure or close contact with an infected person. Pre-exposure prophylaxis is not available in the US. A killed cell vaccine is said to be available in the UK. Usually will become non-infective after several days of antimicrobial therapy.

Plague-18 Nursing considerations:
Standard and droplet isolation precautions should be used for the pneumonic type and the ??? continued until sputum is negative. Standard and contact precautions used for bubonic if open wounds unless progression to lungs occurs. Avoid contact with drainage. See module on infection control or CDC site for details.

Plague-19 Nursing considerations cont.:
Supportive nursing care varies according to type and symptoms and includes appropriate information to patients, family and staff about: Information on infection control (included in another module as is instruction on large-scale outbreak management). Consider emotional impact of word, “plague.” On first patient contact with possible plague case, assess travel history, animal contacts and any infected insect bites especially from fleas.

Smallpox (Variola virus)
Description and Etiology: Caused by the variola virus, a DNA virus member of the orthopox virus family. Other orthopoxes include monkeypox, camelpox and chickenpox. Epidemiology: The last natural human case of smallpox occurred in 1977 in Somalia. No animal reservoir has been identified. Identification of even one case of smallpox constitutes an international public health emergency.

Smallpox-2 Transmission: Incubation: Droplet Aerosol
Direct person-to-person contact including skin lesions and secretions or Through contact with contaminated linens, clothing, surfaces, and other fomites Smallpox is highly contagious Incubation: Typically 12 to 14 days after infection but can be 7 to 17 days. The person may be contagious during prodrome phase and is most contagious as rash forms. Is contagious until all scabs are gone. Typically virus is transmitted from an infected person by coughing or sneezing to the oral mucosa of a susceptible person.

Smallpox-3 Clinical manifestations:
Usually begins with the flu-like symptoms of fever (typically 101o to 103o F), malaise, headache, and body aches (prodrome). In most people, about 90% develop a rash first as red spots on tongue and in mouth which develop into sores in mouth. A rash starts on face, then to arms and legs and hands and feet within 24 hours. Over days, the rash becomes raised bumps which fill with opaque fluid and have a depression in center (said to look like a belly button).

Smallpox-4 Picture from CDC

Smallpox-5 Clinical manifestations cont.:
Bumps become pustules (often said to feel like BB pellets embedded). The pustules crust over to form scabs. The scabs generally fall off after about a total of 3 weeks after the rash first appeared. Pitted scars are left at site of scabs. Lesions are generally round and 6-10 mm. in diameter with concentration on face and extremities.

May be distributed in a centrifugal pattern. In some 5-10% of patients, a hemorrhagic form occurs during which the erythematous lesions are confluent, and the skin is said to look like crepe rubber. There may be bleeding into the skin with petechiae and ecchymoses. This form is usually fatal within a week.

There is also a flat type with an atypical rash that never becomes pustules and has a high mortality. Less severe forms may occur in those with partial immunity from vaccination. Note: In contrast to chickenpox, smallpox skin lesions in the same area develop at same pace and appear similar while in chickenpox, the lesions develop in crops and lesions that are scales, vesicles and pustules may be seen simultaneously. Chickenpox lesions are rarely seen on palms of hands or soles of feet.

Smallpox-8 Diagnosis: Mortality: Treatment:
Sample from lesion should be taken by a recently vaccinated health care worker under appropriate precautions. Mortality: About 30%. Treatment: Supportive including hydration, sedation and pain management. Cidofovir may be promising. Post-exposure vaccination if given within 2 to 3 or possibly up to 5 days post-exposure may prevent or ameliorate disease.

Smallpox-9 Management and nursing considerations: Supportive.
Appropriate infection control critical. The smallpox virus is small in size and can be carried by air currents or on dust particles over long distances and thus be transmitted to susceptible persons in a small amount of time. An actual or suspected case of smallpox should be treated as a public health emergency and reported as appropriate in the staff member’s institution per their disaster plan.

Smallpox-10 Management and nursing considerations cont.:
Should use immediate isolation of suspected case with airborne, contact, and standard precautions and barrier nursing. Individual room with negative air pressure is desirable. In places where no negative pressure isolation rooms exist, the patient should be put in a private room with a HEPA filtration unit.

The patient should remain in their room with doors and windows closed. If there are a large number of patients needing care, a designated nursing unit may be created with a barrier plan to seal off the existing ventilation system from other hospital areas and limiting access to the unit. In cases of mass numbers, a whole facility or large gym may be dedicated to smallpox cases.

Unvaccinated visitors should remain at home until vaccinated. Health care workers should use the personal protective equipment (PPE) appropriate to the degree of exposure and tasks. Disposable N95 respirators that filter particles to 0.02 microns or powered air-purifying respirators should be worn when entering the room, and removed after leaving. Unless absolutely necessary, the smallpox patient should not leave their room.

If the patient must leave their room, they should wear a N-100 mask, have their body completely covered, including the head and face (nose and mouth should not be covered) except with mask. Hallways should be cleared and anyone with the patient should wear PPE including N95 respirators. Use disposable patient care equipment and dedicated non-disposable equipment.

Linens should be placed in one bag, sealed and then placed in a second leak-proof bag with clear identification as contaminated and chutes should not be used. If patient dies, they should be placed in leak-proof container. Specific infection control information is in another module or can be found on the CDC website. Provide psychological support to patient and family. Unvaccinated personnel should not care for smallpox patients if an immune healthcare worker is available.

Smallpox-15 Vaccination: Available.
Uses vaccinia virus for vaccination. Complications of vaccination occur particularly in immunocompromised persons. Post-exposure vaccination may be useful. See above. Passive immunization with vaccine immunoglobulin may be given especially if more than 3 days have elapsed since exposure.

Smallpox-16 Vaccination cont.:
Vaccination often performed for contacts as ring vaccination. In this model, contacts of the patients are identified and vaccinated with further case identification, surveillance contact identification and vaccination in concentric “rings.” This has been proposed rather than universal vaccination in which many more reactions to the vaccine would be seen.

Smallpox-17 Other notes: Requires biosafety level 4.
Staff caring for patients with smallpox may be asked to monitor their temperatures daily, not use main hospital entrance, shower and change before leaving and not enter main hospital area during work. Some recommend not admitting smallpox patients to hospitals but maintaining them in the home because smallpox is so contagious that hospitalization could increase the number of people at potential risk of transmission.

Tularemia (Francisella tularensis)
Description: Is a category A agent because of infectivity, ease of dissemination, and ability to cause serious illness. Other names: Deer-fly fever, Glandular tick fever, Market man’s disease, Rabbit fever, and O’Hara’s disease

Tularemia-2 Etiology: Francisella tularensis, a tiny, gram-negative, non-spore forming, hardy, aerobic coccobacillus. Two subspecies: Type A is more common in North America and is more virulent than Type B, found in Asia, Europe and North America. Type A typically associated with rabbits. Type B typically associated with rodents or wet environment.

Tularemia-3 Epidemiology: A zoonotic infection.
Occurs in the US, Europe, and Asia. Has diverse small mammal animal hosts, including rabbits, squirrels, muskrats, mice, water rats, and others that are natural reservoirs of infection. F. tularensis may be recovered from soil, water, and vegetation. In the US, fewer than 200 recognized cases occur each year. Disease is endemic in Martha’s Vineyard. Is occupational risk for hunters, trappers, and others who handle infected animal carcasses.

Tularemia-4 Transmission:
Direct contact with infected animal fluids or tissues, Ingestion of contaminated water, Ingestion of contaminated undercooked meat, water or soil, Bites of infected arthropods, such as ticks, Inhalation of infectious aerosols, such as contaminated dust, or deliberate release in laboratory, or Direct contact with contaminated food, water, or soil. Person-to-person spread is unusual.

Tularemia-5 Incubation period: Clinical manifestations:
1 to 21 days, typically 3 to 5 days Clinical manifestations: Extremely variable depending on type, route of inoculation and dose. Occurs in six recognized clinical forms: ulceroglandular, glandular, oculoglandular, oropharyngeal, pneumonic, and typhoidal. Tularemia sepsis may follow dissemination and be severe leading to disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), and organ failure if not treated immediately and appropriately.

Tularemia-6 Clinical manifestations cont.:
Ulceroglandular – is the most common type. Occurs following the bite of an infected arthropod or handling an infected animal. Begins as chills, fever, headache, generalized aches, and can disseminate to lymph nodes, and their enlargement or lymphadenopathy may resemble buboes in bubonic plague. A skin papule develops that becomes pustular and eventually ulcerates. The skin lesion can last for months.

Tularemia-7

Glandular – similar to above but without the ulcer. Oculoglandular – occurs after eye contamination causing conjunctival ulceration, inflamed eyelids and nodules, vasculitis and possibly regional lymphadenopathy Oropharyngeal – occurs after ingestion of contaminated food or water. Results in pharyngitis with yellow-white pseudomembrane, and tonsillitis with cervical or retropharyngeal lymphadenopathy. In some cases, diarrhea and bowel ulceration may occur.

Pneumonic (primary) – from inhaling infected aerosols. Can present as atypical pneumonia or present as acute illness with fever, fatigue, chills, headache and malaise. Cough, usually nonproductive, manifestations of bronchitis, pneumonitis, chest pain and dyspnea may occur. Erythema multiforme may occur, and a rash or erythema nodosum may be seen in about one-third.

Typhoidal – acute septicemic illness with fever and prostration leading to delirium without skin lesion or lympohadenopathy. Pneumonia is common. May exhibit abdominal pain, vomiting and diarrhea. Mortality rate is about 35% to 60%.

Tularemia-11 Diagnosis: Mortality: Clinical suspicion.
Serological testing, culture sputum for gram stain culture and other testing. Identification of organism in other tissues as appropriate. Mortality: If untreated, ranges from 5% to 35%, overall. With prompt treatment may be only 1%.

Tularemia-12 Treatment:
Preferred treatment is parenteral streptomycin or intravenous gentamicin or aminoglycosides for 10 days. Fluoroquinolones show promise in treatment. In a mass casualty situation, doxycycline and ciprofloxacin given orally is recommended. Postexposure prophylaxis with ciprofloxacin or doxycycline for 14 days is recommended to prevent clinical disease if begun during the incubation period.

Tularemia-13 Nursing considerations: Vaccine: Other:
Standard isolation precautions are recommended. Supportive care. Vaccine: One form was available and recommended for certain occupations but some difficulties were found. The live attenuated vaccine is still being investigated. Other: Studied in biosafety lab 3. For laboratory workers, negative pressure microbiological cabinets as well as face masks are recommended.

Tularemia-14 Prevention: In natural cases: Avoid tick-infested areas
Avoid tick and mosquito bites through protective clothing, repellents, tick checks. Use gloves, masks, protective eye-cover when handling wild animals. Cook wild game thoroughly. Avoid drinking untreated water.

Other Hemorrhagic Fever Arenaviruses
The category includes 5 arenaviruses that cause viral hemorrhagic fevers. Lassa virus (Lassa fever), which is one of these, is discussed separately in this module. Other arenaviruses and the viral hemorrhagic fevers they can cause include: Virus Disease Junin virus Argentine hemorrhagic fever Sabia virus Brazilian hemorrhagic fever Machupo virus Bolivian hemorrhagic fever Guanarito virus Venezuelan hemorrhagic fever

SAHF-2 These four viruses are sometimes known collectively as South American hemorrhagic fever (SAHF) viruses and are discussed collectively first. Then Junin virus causing Argentine hemorrhagic fever is discussed specifically next along with information about the other SAHF viruses. The SAHF viruses each cause diseases of similar symptomatology. Specific species of rodents are natural hosts for the viruses. The typical incubation period is 7 to 14 days but may extend from 5 to 21 days. Case fatality rates are estimated as 15 to 30%.

SAHF-3 Rodents are implicated in transmission through contaminated food, water or direct contact with infected secretions or through inhalation of infectious secretions or excretions such as infected rodent urine. Person-to-person transmission may occur especially for Machupo virus.

SAHF-4 Clinical features tend to be similar with:
Gradual onset of fever Malaise followed by myalgia, back pain, headache and dizziness with hyperesthesia of the skin Hemorrhagic manifestations include hemorrhaging from gums, vagina and gastrointestinal tract leading to hypovolemic shock Neurological manifestations include tremors, inability to swallow, grand mal convulsions and coma.

SAHF-5 Clinical features cont.:
Some symptoms are more specifically associated with individual viruses. For example, in Guanarito virus, pharyngitis, vomiting, and diarrhea are more commonly seen. In Junin and Machupo viral infections, petechiae, erythema, facial edema, hyperesthesia of the skin and shock may be more frequent. Both of these have a high fetal mortality if occurring in pregnant women.

SAHF-6 Clinical features noted during an outbreak of Venezuelan hemorrhagic fever included fever, conjunctivitis, pharyngitis, thrombocytopenia, myalgia, and hemorrhagic manifestations. Facial edema was also observed. In this outbreak, 9 of 15 cases died. A few hundred cases have been reported. Clinical features noted in an outbreak of Bolivian hemorrhagic fever included: fever, chills, malaise, arthralgias, severe lower back pain, headache and hemorrhagic manifestations. The incubation period was 1 to 2 weeks. The case fatality rate is estimated at 20%. Nosocomial transmission has been noted.

SAHF-7 If used for bioterrorism, viremia may be high with a higher transmission rate and higher mortality as well as a greater frequency of secondary cases because of the large number of patients flowing into emergency facilities due to nosocomial transmission. Standard, contact and airborne isolation precautions. Barrier nursing precautions as outlined for Lassa fever should be followed. Biosafety containment level 4 is used for these viruses.

Junin Virus & SAHF Viruses
Etiology: Junin virus is a RNA virus in the arenavirus family. It belongs to what is commonly known as the New World arenaviruses-Machupo virus, Guanarito virus and Sabia virus. Each of these can cause a viral hemorrhagic fever similar to the Argentine hemorrhagic fever caused by Junin virus.

Junin Virus & SAHF Viruses -2
Epidemiology: Junin and other new world viruses have mostly been identified from the 1950s to date. The natural hosts are rodents. The at-risk region is mainly Argentina. It tends to be seasonal with a peak during the corn harvest from March to June. Most of those infected are agricultural workers who inhale infected aerosols from rodent excreta or when rodents are caught in mechanical harvesters. Aerosol infections have been noted in laboratory workers. Sabia virus infection has only been documented rarely. In one case, it was laboratory acquired in the US and the researcher was treated with ribavirin and survived.

Transmission: Contact with infected rodents, inhalation of infectious rodent secretions or excretions. Person-to-person airborne spread has been described for Machupo virus as well as Lassa virus (discussed earlier). Machupo virus has been transmitted to spouses 1-3 weeks after onset of illness. Nosocomial transmission mediated by infected blood and excretion contact is described as possible as is contact with medical equipment that has been contaminated by virus.

Incubation period: Typically 7 to 14 days, but can be 2 to 21 days. Clinical manifestations: Are similar but not identical for the South American hemorrhagic fevers. Typical onset is gradual with fever, malaise followed by headache, myalgia, back pain, dizziness, and hyperesthesia of the skin. Guanarito virus infections tend to include pharyngitis, vomiting and diarrhea more frequently than others.

Clinical manifestations cont.: Junin and Machupo infections tend to include petechiae, erythema and flushing of face and trunk, facial edema and lymphadenopathy. Hemorrhagic and neurological manifestations may occur alone or together. Hemorrhagic manifestations include hemorrhaging from the gums and orifices, especially the gastrointestinal tract and vagina in females leading to shock, and capillary leak syndrome with thrombocytopenia.

Clinical manifestations cont.: Neurological manifestations include tremors, inability to swallow, dysarthria, convulsions, coma and death which may occur 7 to 12 days after onset. Recovery is usually complete but there may be a temporary loss of scalp hair. Pregnant women are more likely to have a fatal outcome if infected with Junin virus and both Junin and Machupo viruses are associated with high fetal mortality.

Mortality: Mortality rate is 15-30%. Treatment: Ribavirin as been used successfully intravenously for about 10 days, and is recommended for at-risk contacts orally for a week. Limited number of studies are available though. Other treatment is generally non-specific and supportive, including fluid and electrolyte balance, monitoring, and clotting factor or platelet replacement may be done in cases of serious hemorrhage. Convalescent or immune serum therapy has been used for Junin and Machupo viral infections.

Nursing considerations: Strict barrier nursing precautions should be used, including standard and contact isolation precautions, and in the interests of absolute safety, airborne precautions. Educate patient about isolation precautions being used. Indicate what is expected of them in regard to cooperation if they are able to cooperate and understand. See infection control module for details and CDC site as well as material previously discussed under Lassa, Ebola and Marburg viruses. Supportive care.

Other notes: Biosafety level 4 conditions are used for study. Picture from CDC.

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