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MD Consult: Books: Goldman: Cecil Medicine: Chapter 19 – BIOTERRORISM

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier

Chapter 19 – BIOTERRORISM

John G. Bartlett

BIOLOGIC WEAPONS

Definition

Weapons of mass destruction are classified as biologic, chemical, or nuclear. Biologic weapons are microbes or microbial products that are used for bioterrorism. The potential for mass destruction is evident from a report from the U.S. Office of Technology, which predicted that release of 100 kg of anthrax spores upwind of Washington, DC, would cause 130,000 to 3,000,000 deaths, thus matching the lethal potential of a hydrogen bomb.

Epidemiology

Despite the enormous potential for mass destruction, the reality is that the actual application of bioterrorism has been quite limited. During World War II, there were major bioweapon programs in the United States, the Soviet Union, Japan, and Germany, but only Japan used it in any well-established way. The largest bioweapon program was by the Soviet Union, which had approximately 50 facilities and 60,000 employees. In 1972, the Biologic and Toxin Weapons Convention, which was established to eliminate the threat of bioterrorism, was signed by 140 nations, including the United States and the Soviet Union. The subsequent destiny of the enormous volume of products (smallpox virus, botulinum toxin, anthrax spores, etc.) and most of the scientists who were highly skilled in this area is largely unknown. Current estimates are that many nations continue to harbor bioweapon programs.

In addition to these large-scale national programs, there is also the potential for use of bioweapons by individuals or dissident groups. For example, in 1984 a religious cult in Oregon attempted to influence an election by contaminating restaurant salad bars with Salmonella to reduce voter turnout; the effort resulted in 751 cases of salmonellosis, but the election was not affected. Aum Shinrykio, a Japanese cult, was responsible for the release of sarin nerve gas in Tokyo, which resulted in 6000 casualties and 10 deaths.

More recently, there were 22 cases of anthrax in the United States during a 2-month period in 2001 as a result of contaminated letters sent to four sites. Of the 22 cases, 20 were traced directly to contaminated mail, all with the same molecular type of Bacillus anthracis. Some cases were cutaneous because the contaminated material in letters was milled to a relatively large particle size that contaminated surfaces via gravity. By contrast, letters with anthrax that was milled to nearly the size of a single spore resulted in particles that were aerosolized at release and inhaled, thereby causing inhalational anthrax. Exposed persons were advised to receive prophylactic doxycycline or ciprofloxacin, and in none of more than 10,000 persons who received even a single dose of either antibiotic did anthrax subsequently develop. For this terrorist act, the U.S. Centers for Disease Control and Prevention (CDC) assigned more than 1000 personnel to the epidemic and still needed more. In a 1-month period, the New York City Health Department managed over 15,000 telephone inquiries. During the outbreak, more than 200 mailed or telephoned threats of bioterrorism were recorded. Thus, despite a relatively small incident with just 22 cases over a 2-month period, the impact on society and health care resources was enormous.

Classification

The agents of bioterrorism are classified as A (greatest potential; Tables 19-1 and 19-2 [1] [2]), B (less likely or important), or C (not believed to be a high bioterrorism risk). This classification is based on the following criteria:

   1.    Impact on public health in terms of illness and death
   2.    Ease of delivery based on stability of the agent and ability to mass produce and distribute
   3.    Potential for person-to-person transmission
   4.    Public perception in terms of potential for civil disruption
   5.    Requirements for a special public health response


TABLE 19-1   — 
CLASSIFICATION OF BIOTERRORISM AGENTS

  Public Health Impact Dissemination[*]    
Agent Disease Death Delivery Potential Person to Person Public Perception[] Special Preparation[]
Smallpox (A) + ++ + +++ +++ +++
Anthrax (A) ++ +++ +++ 0 +++ +++
Plague (A) ++ +++ ++ + ++ +++
Botulism (A) ++ +++ ++ 0 ++ +++
Tularemia (A) ++ ++ + 0 + +++
Viral hemorrhagic fever (A) ++ +++ + ++ +++ ++
Viral encephalitis (B) ++ + + 0 ++ ++
Q fever (B) + + ++ 0 + ++
Brucellosis (B) + + ++ 0 + ++
Glanders (B) ++ +++ ++ 0 0 ++
Melioidosis (B) + + ++ 0 0 ++
Psittacosis (B) + + ++ 0 0 +
Ricin toxin (B) ++ ++ ++ 0 0 ++
Typhus (B) + + ++ 0 0 +
Cholera (B) + + ++ +/- +++ +
Shigellosis (B) + + ++ + + +

+++, Death in more than 50%; ++, 21 to 49%; +, less than 20%.

A = Greatest potential for bioterrorism; B = less likely or important for bioterrorism.

* Potential for rapid large-scale dissemination.
Media reports with +++ include more than 45 titles in surveying 233 newspapers and 70TV/radio sources.
Needs therapeutics, surveillance, laboratory demands.


TABLE 19-2   — 
CLINICAL FEATURES OF CATEGORY A AGENTS

  Anthrax (Inhalation) Smallpox Plague (Pneumonia) Tularemia Botulism Viral Hemorrhagic Fever
Cases in U.S. per year 0 0 8–10 100–200 100–200 0
Clinical features Flulike, then shock Fever, then characteristic rash Pneumonia, hemoptysis Pneumonia Descending paralysis and involvement of cranial nerves Hemorrhage and fever
Diagnosis Blood culture, CT of the chest BSL-4 laboratory for virus Blood and sputum culture Sputum culture and radiograph Toxin assay of blood, GI specimens; EMG BSL-4 laboratory for virus
Mortality 40–50% 30% 10–20% 1–2% 60% Variable
Treatment[*] Cipro, Doxy, or Levo + 2nd agent,[] 60–100 days None Gent/Strep (Cipro/Doxy), 10 days Gent/Strep (Cipro/Doxy), 10 days Antitoxin, ventilator Ribavirin (some), 7 days
Prevention[*] Cipro/Doxy Vaccine Cipro/Doxy Cipro/Doxy None None
Infection control Not transmitted Contact and airborne precautions Masks Not transmitted Not transmitted Contact precautions

BSL = Biologic Safety Level; Cipro = ciprofloxacin; CT = computed tomography; EMG = electromyography; GI = gastrointestinal; Levo = levofloxacin; Doxy = doxycycline; Gent = gentamicin; Strep = streptomycin; () = alternative to preferred.

* Doses: Ciprofloxacin, 400 mg IV q8–12h or 500–750 mg PO bid; levofloxacin, 500–750 mg IV qd or 500 mg PO qd; doxycycline, 100 mg PO or IV bid; gentamicin, 5 mg/kg/day IM or IV; streptomycin, 1 g IM bid; ribavirin, 16 mg/kg/day IV × 4 days, then 8 mg/kg/day × 3 days or 1000–1200 mg/day PO × 7.
Imipenem (500 mg IV q6h), rifampin (600 mg IV or PO qd), chloramphenicol (1 g IV q6h), clarithromycin (500 mg PO bid), vancomycin (1 g IV bid), or clindamycin (600 mg IV q8h).

   Anthrax

Definition

Infection is caused by B. anthracis ( Chapter 317 ). The three recognized forms that reflect the portal of entry are inhalation, cutaneous exposure, and ingestion.

Epidemiology

The greatest concern for bioterrorism is the inhaled form, which results from the inhalation of B. anthracis spores and results in a devastating disease with a mortality rate of about 50% even with optimal management. The last naturally occurring case of inhalational anthrax in the United States was in 1976. The largest epidemic followed an accidental release of anthrax in Sverdlovsk, Russia, in 1979 and resulted in an estimated 80 to 250 cases. Cutaneous anthrax is the usual naturally occurring zoonotic form. An average of less than 1 case per year now occurs in the United States, with about 2000 naturally occurring cases in the world per year.

Pathobiology

With inhalational anthrax associated with bioterrorism, spores must be milled to less than 5 μm to permit both aerosolization and inhalation. The spores are taken up by alveolar macrophages and migrate to the mediastinal lymph nodes, where they revert to vegetative forms and produce toxins. The protective antigen combines with lethal toxin and edema toxin; these toxins are thought to account for the clinical features.

Clinical Manifestations

The incubation period is usually 4 to 5 days, but the range is from 2 to 43 days after exposure. Inhalational anthrax is a two-stage disease. The initial symptoms are nonspecific and flulike. Features that distinguish this stage from influenza are the lack of coryza and the anticipated exposure history. The second stage is profound sepsis with chest pain, chest compression from large pleural effusions and mediastinal expansion, multiple organ failure, obtundation, cyanosis, hypotension, and death, which may occur within hours. Cutaneous anthrax is characterized by a vesicle that progress to an eschar associated with substantial surrounding edema, often with regional adenopathy and systemic signs of infection.

Diagnosis

The diagnosis is established by recovery of B. anthracis from blood or the infected site. Virtually all patients with inhalational anthrax have positive blood cultures, frequently within 12 to 16 hours if cultures were obtained before therapy. Other highly characteristic features of the disease are a chest radiograph that shows a wide mediastinum and a computed tomography scan that shows hyperdense hilar and mediastinal lymph nodes, often with large pleural effusions. A highly characteristic feature of the disease is large bloody pleural collections. There may or may not be a pulmonary infiltrate.

Treatment

The most important facets of treatment of inhalational anthrax are supportive care, drainage of pleural effusions, and rapid administration of antibiotics. The drugs approved by the Food and Drug Administration (FDA) for B. anthracis are intravenous penicillin, doxycycline, ciprofloxacin, and levofloxacin ( Table 19-2 ). Because no therapeutic trials have been conducted, these drugs are approved on the basis of efficacy shown in a primate model of inhalational anthrax. In reality, a bioterrorism event with inhaled anthrax will result in specific recommendations from the CDC. In 2001, the preferred agents were doxycycline or ciprofloxacin combined with a second agent such as penicillin, imipenem, rifampin, chloramphenicol, clarithromycin, vancomycin, or clindamycin based on sensitivity tests of the epidemic strain. After clinical improvement, the intravenous administration may be changed to oral agents such as ciprofloxacin, levofloxacin, or doxycycline; the total recommended duration of treatment is 60 to 100 days. The prolonged course is suggested because studies in primates show persistence of spores after drugs were given for up to 30 days. For cutaneous anthrax, the recommendation is ciprofloxacin or doxycycline for a total of 60 to 100 days because of the assumption that a patient with cutaneous anthrax as a result of bioterrorism may have inhaled organisms as well.

Prevention

In the event of bioterrorism, prophylaxis appears to be critical because it is nearly 100% effective, whereas patients in whom the disease develops have substantial morbidity and mortality despite optimal management. During the 2001 epidemic, the recommendation was oral doxycycline or ciprofloxacin for 60 to 100 days; despite variable compliance, anthrax did not develop in any individual. An FDA-approved anthrax vaccine given in six administrations to wool sorters and other workers in high-risk occupations is highly effective, but other forms of anthrax vaccine are now being developed in the hope that they will require fewer administrations and have less adverse reactions.

Prognosis

Available data from the Sverdlovsk outbreak in Russia suggest a mortality rate of 60 to 87% despite appropriate antibiotics. In the 2001 epidemic in the United States there were five deaths (45%) in 11 patients despite aggressive management. In fatal cases, the interval between the onset of symptoms and death averaged 3 to 4 days.

   Smallpox

Definition

Smallpox is a systemic infection caused by the virus Variola major or Variola minor ( Chapter 395 ). The assumption is that any attempt at bioterrorism with smallpox would use V. major, which is associated with a substantially higher mortality rate. The virus is viewed as ideal for bioterrorism because it is easy to culture, survives well in aerosols, and is lethal in of 30% of cases. Furthermore, most humans are now susceptible because immunization was stopped in the United States and most of the world by 1973.

Epidemiology

The global campaign to eradicate smallpox was initiated in 1966, and the last naturally occurring case was reported in 1977. In 1980 the World Health Organization (WHO) declared smallpox eradicated and recommended that all laboratories destroy stocks of variola or transfer them to one of two WHO reference laboratories, one in Moscow and the other at the CDC in Atlanta. These remaining isolates were to be destroyed in 1999, but the WHO agreed to retain the supplies in an effort to develop an attenuated vaccine and antiviral drugs. The number of countries that have this virus other than Russia and the United States is not known.

Smallpox is spread from person to person in droplets from the oral pharynx. The greatest risk is to persons within 6 to 8 feet of an infected individual, and prior epidemics have consistently shown that most cases occur in household members and hospital contacts. The secondary attack rate in unvaccinated household members is 37 to 88%. Because the disease has been eradicated, any confirmed case of smallpox implies bioterrorism.

Clinical Manifestations

The incubation period is usually 12 to 14 days. Initial symptoms are high fever, malaise, prostration, headache, and backache. These symptoms are severe, and most patients are bedridden. The rash usually appears on day 3 as a maculopapular eruption that subsequently evolves through the vesicular and then pustular stages; at 2 to 3 weeks it forms scabs that separate and leave a characteristic pitted scar. The rash begins on the face and forearms and then spreads to the trunk and legs. Pustules have a characteristic firm, round, deep-seated appearance and measure 7 to 10 mm in diameter. Lesions are more dense on the face and extremities, all are in the same stage, and there may be involvement of the palms and soles. An important issue in terms of disease control is that transmission takes place during the rash phase and not during the early pre-rash period of illness.

Diagnosis

Laboratory diagnosis requires fluid collected from a typical vesicular or pustular lesion, preferably by a vaccinated person with appropriate protection. Laboratory testing must be done in a maximum containment facility (Biologic Safety Level 4 [BSL-4] laboratory); tissue culture is used to recover the virus, and polymerase chain reaction and restriction fragment length polymorphism are used to characterize the viral strain. For the clinician, the major issue is the distinction of smallpox from chickenpox or other illnesses that are also characterized by a vesicular rash ( Table 19-3 ). With chickenpox ( Chapter 398 ), the lesions are more superficial, have a centripetal distribution with more involvement of the trunk and face, and are not all at the same stage of evolution. Patients are also less seriously ill.


TABLE 19-3   — 
MAJOR AND MINOR CRITERIA FOR SMALLPOX AND PRIORITY FOR REPORTING TO THE CENTERS FOR DISEASE CONTROL AND PREVENTION

MAJOR CRITERIA:
Fever (>38.3°C) 1–4 days before the onset of rash plus one of the following: headache, prostration, chills, vomiting, and abdominal pain
Typical smallpox lesions: firm, round, deep-seated vesicles or pustules with evolution to become umbilicated or confluent
Lesions same stage in development
MINOR CRITERIA:
Centrifugal distribution of the rash (face and extremities)
First lesions on oral mucosa, palate, face, and arms
Patient appears toxic or moribund
Slow evolution of lesions—each stage lasts at least 1–2 days
Lesions on palms and soles
REPORTING PRIORITY:
Report immediately: (1) febrile prodrome, (2) classic smallpox lesions, and (3) lesions in the same stage of development (need all 3)
Urgent assessment: (1) febrile prodrome and one other major smallpox criterion or (2) febrile prodrome plus ≥4 minor criteria
Manage as clinically indicated: febrile prodrome and ≥4 minor criteria

Other conditions in the differential diagnosis for a vesicular or pustular rash include disseminated herpes zoster or herpes simplex ( Chapter 397 ), drug eruptions ( Chapter 466 ), erythema multiforme ( Chapter 464 ), enteroviral infection ( Chapter 402 ), secondary syphilis ( Chapter 340 ), monkeypox ( Chapter 395 ), molluscum contagiosum ( Chapter 464 ), and generalized vaccinia. With a generalized maculopapular rash, the differential diagnosis includes measles ( Chapter 390 ), rubella ( Chapter 391 ), drug rash, erythema multiforme, and scarlet fever ( Chapter 311 ).

Treatment

There is no therapy with established merit.

Prevention

Vaccination with vaccinia (cowpox) virus before exposure provides significant protection against smallpox. Persons in whom a vesicle or pustule develops or who have a pitted scar at a previous vaccination site have “a take” indicating an immune response. The duration of protection is not well known. Vaccination also provides some protection when given within 4 days after exposure because the immune response to vaccinia is faster than it is to smallpox. The major goal in the event of anticipated bioterrorism is to vaccinate persons with anticipated risks, such as military personnel or hospital-based smallpox response teams. In an outbreak, the highest priority will be first responders, household contacts, and others who have face-to-face contact with patients after the onset of fever.

Vaccination was associated with substantial risk when it was given routinely before 1973. The major currently recognized vaccine-associated complications ( Chapter 16 ) include (1) postvaccinal encephalitis, which is probably a immune reaction; (2) progressive vaccinia, which is a progressive and rapidly lethal complication of disseminated vaccinia seen primarily in patients with defective cell-mediated immunity; (3) generalized vaccinia caused by dissemination of vaccinia; (4) accidental inoculation of other anatomic sites or other persons, usually bedmates; and (5) eczema vaccinatum in patients with a current or past history of eczema or atopic dermatitis. Complications that result from uncontrolled growth of vaccinia can be treated with vaccinia immune globulin. During the recent experience with smallpox vaccination in more than 500,000 U.S. military personnel and health care workers, the frequency of these adverse reactions was modest and no deaths were recorded; however, another major complication was recognized: myopericarditis, which was most common with primary vaccination, self-limited, and probably immune mediated.

   Plague

Definition

Plague refers to infection by Yersinia pestis ( Chapter 333 ).

Epidemiology

Approximately 10 cases of plague occur in the United States annually, but the pneumonic form of disease that would be anticipated in the event of bioterrorism is rare, with only about 7 cases in the past 50 years. Thus, any case of pneumonic plague, particularly if acquired in urban areas and outside endemic areas, should arouse suspicion of bioterrorism. An important clinical clue to the diagnosis is severe pneumonia associated with hemoptysis. It is known that Y. pestis was produced in large quantities by Soviet scientists for bioterrorism before abandoning this program in 1992. The WHO has estimated that a 50-kg release of Y. pestis over an urban area of 5 million people would result in 150,000 cases of plague pneumonia and 36,000 deaths.

Clinical Manifestations

The incubation period is 1 to 6 days. The pneumonic form is associated with bloody sputum, fever, dyspnea, and frequently gastrointestinal symptoms, including nausea, vomiting, abdominal pain, and diarrhea. The course is rapidly progressive with a sepsis syndrome at 2 to 6 days. Chest radiographs usually show consolidated infiltrates, and about 50% of patients have pleural effusions.

Diagnosis

Y. pestis is a gram-negative coccobacillus that demonstrates bipolar staining and resembles a safety pin. Although the organism may be recognized by Gram stain of sputum, most laboratories require extended periods to identify it with standard methods. If this diagnosis is suspected, the laboratory should be warned so that one culture can be incubated at 28° C for rapid growth and a second at 37° C to permit identification of the capsular antigen. Rapid diagnostic tests are available in some state health departments, the CDC, and some military facilities. The differential diagnosis includes other severe forms of pneumonia or epidemic pneumonia, such as legionnaires’ disease ( Chapter 335 ), histoplasmosis ( Chapter 353 ), anthrax ( Chapter 317 ), tularemia ( Chapter 332 ), and influenza ( Chapter 387 ).

Treatment

The preferred drugs are streptomycin or gentamicin; doxycycline and fluoroquinolones such as ciprofloxacin or levofloxacin are alternative agents. The duration of treatment is 10 days.

Prevention

Limited data define the efficiency of person-to-person transmission. Current recommendations are for contact and droplet precautions with the use of masks, gowns, gloves, and eye protection. Isolation may be discontinued after 48 hours of antibiotic treatment and clinical improvement. Prophylactic doxycycline or ciprofloxacin is recommended for 7 days for household members, health care workers, and other close contacts of patients. Prophylactic antibiotics are also advocated for other persons with a common-source exposure. Like anthrax, prophylaxis is virtually 100% effective, whereas treatment after the onset of symptoms is much less successful.

Prognosis

The fatality rate of pneumonic plague approaches 100% without therapy. Mortality has been reduced to 5 to 14% with aminoglycoside treatment, but this experience is based largely on syndromes that are generally less severe than plague pneumonia.

   Botulism

See Chapter 319 .

   Tularemia

Definition

Tularemia is an infection caused by Francisella tularensis ( Chapter 332 ).

Epidemiology

About 100 to 200 cases of tularemia are diagnosed per year in the United States, primarily in rural areas, especially in Oklahoma, Arkansas, Missouri, South Dakota, and Montana. Since 2000, there have been more than 15 cases in Martha’s Vineyard in Massachusetts. With bioterrorism, the expectation would be a large number of cases of acute nonspecific febrile illness with pneumonitis. However, aerosol delivery could result in multiple other forms, depending on the anatomic site of inoculation, including ulceroglandular (from contaminated wounds), ocular, and oropharyngeal tularemia.

Clinical Manifestations

The incubation period is 3 to 5 days. The illness is characterized by fever, sometimes with a temperature-pulse disassociation, and progresses to pharyngitis, bronchitis, and pneumonitis with pleurisy and hilar adenopathy. When compared with plague or anthrax, inhalational tularemia progresses much more slowly and has a low fatality rate. Other manifestations include pharyngeal (exudative pharyngitis with fever and cervical adenopathy) and typhoidal (fever prostration and septic shock) tularemia.

Diagnosis

The chest radiograph typically shows hilar adenopathy. Respiratory secretions contain small gram-negative coccobacilli but not the “safety pin” form of plague. The diagnosis is established by direct immunofluorescent antibody staining, but the reagents are available only from specialized laboratories in the Laboratory Response Network. The organism may be used, but the laboratory must be warned for two reasons: to use specialized media and to take special precautions to avoid exposure. Growth is slow, with 2 to 5 days generally required.

Treatment

The preferred drugs are streptomycin or gentamicin given for 10 days; doxycycline and ciprofloxacin are alternatives. Exposed persons in whom fever develops within 14 days of exposure should be treated expectantly.

Prevention

The preferred antibiotic for postexposure prophylaxis is doxycycline or ciprofloxacin given for 14 days. There is no person-to-person spread, so health care workers, family members, and other close contacts with cases are at no risk.

   Viral Hemorrhagic Fever

Definition

The hemorrhagic fever viruses include diverse organisms that cause a clinical illness characterized by fever and bleeding. These agents are grouped in four families: Filoviridae, Arenaviridae, Bunyaviridae, and Flaviviridae ( Table 19-4 ). These viruses are attractive for bioweapons because the minimum infecting dose may be as low as 10 virions, they can be distributed by aerosols, mortality rates are virus dependent but often high, they generate great fear, many are transmitted person to person, and no good treatment is available.


TABLE 19-4   — 
VIRAL HEMORRHAGIC FEVERS

Agent Source Vector Clinical Features P-P Tx Treatment Mortality
Ebola Africa Not known Fever, rash, DIC + Supportive 50–90%
Marburg Africa Not known Fever, rash + Supportive 20–70%
Lassa fever Africa Rodent Fever, conjunctivitis + Ribavirin 15–20%
New World Arenaviridae South America Rodent GI symptoms, conjunctivitis, adenopathy + Ribavirin 15–30%
Rift Valley fever Africa, Saudi Arabia Mosquito Fever, jaundice, photophobia No Ribavirin <1%
Yellow fever Africa, Americas Mosquito Fever, jaundice, conjunctivitis No Supportive 20%
Omsk hemorrhagic fever Central Asia Tick Fever, cough, conjunctivitis, adenopathy No Supportive 1–10%
Kyasanur India Tick Biphasic encephalitis No Supportive 3–10%

DIC = disseminated intravascular coagulation; GI = gastrointestinal; P-P Tx = Person-to-person transmission; + = yes.

Epidemiology

The hemorrhagic fever viruses are not normally found in the United States, Europe, or Australia. They are transmitted by contact with infected animals or arthropod vectors, although the natural reservoir for Ebola and Marburg viruses is not known. Any case of viral hemorrhagic fever in a patient in a nonendemic area who has not visited an endemic area within the previous 22 days is presumed to represent bioterrorism.

Clinical Manifestations

The onset of illness is generally nonspecific and consists of fever and myalgias. Additional symptoms are “virus dependent” ( Table 19-4 ) and include rash, encephalitis, pharyngitis, adenopathy, and gastrointestinal symptoms. The syndrome progresses to thrombocytopenia with petechiae, hematuria, hematemesis, hemoptysis, and melena. Disseminated intravascular coagulation with shock, delirium, convulsions, and coma may then develop.

Diagnosis

Laboratory features include thrombocytopenia, as well as leukopenia, anemia, or hemoconcentration. All specimens from patients with suspected viral hemorrhagic fever should be referred to the CDC for testing in a BSL-4 laboratory. Personnel in the referring laboratory must be warned, and only designated technicians should be assigned to processing.

Treatment

Ribavirin has activity in vitro against Lassa fever virus, New World arenaviruses, and bunyaviruses, but clinical experience is limited. It is assumed that a limited number of cases involving these viruses would permit the use of intravenous ribavirin, but a mass casualty setting would require oral administration. Treatment of other hemorrhagic fever viruses would largely be limited to supportive care.

Prevention

The major concern is nosocomial and household transmission by contact with blood and other body fluids. Patients should be in a single-occupant negative-pressure room, and health care personnel should use N95 respirators or powered air purifying respirators (PAPRs), double gloves, impermeable gowns, goggles or face shields, and leg and shoe coverings. Nonessential staff and visitors should be excluded. Dedicated medical equipment such as stethoscopes and point-of-care analyzers should be available. Laboratory specimens should not be sent in pneumonic systems, contaminated objects should be cleaned with 1:100 household bleach or a similar disinfectant, and contaminated cloth items should be double-bagged and incinerated or autoclaved. Particular care needs to be exercised in managing corpses.

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