Potential weapons of biologic, radiologic, and chemical terrorism

CHAPTER 110


Potential weapons of biologic, radiologic, and chemical terrorism


In the fall of 2001, the United States was hit by unprecedented terrorist attacks. On September 11, terrorists hijacked four commercial jets, and succeeded in crashing two into the twin towers of the World Trade Center and one into the Pentagon. In October, anthrax spores were mailed to several locations, causing illness and death. These events have generated great concern about our vulnerability to more such attacks, and our ability to manage the consequences.


To improve our readiness for a terrorist attack, the federal government has taken several steps, including passage of the Public Health Security and Bioterrorism Preparedness and Response Act of 2002 (the Bioterrorism Act), the Project BioShield Act of 2004, and the Pandemic and All-Hazards Preparedness Act in 2007. All three incentives were designed to spur development and production of drugs and vaccines to protect U.S residents from bioterror agents, such as anthrax, smallpox, botulism, and plague. Although there have been some notable results, much more needs to be done.


In this chapter, we discuss some of the potential weapons of terrorism, focusing primarily on bacteria and viruses. Biotoxins, chemicals (nerve agents and mustard gas), and radiologic weapons are addressed as well. Discussion centers on clinical manifestations and treatment. Prevention is addressed where appropriate.


For more information on the weapons discussed here, or for information on other potential weapons, you can consult the online resources listed in Table 110–1.





Bacteria and viruses


Bacillus anthracis (anthrax)


Bacillus anthracis is the bacterium that causes anthrax, a disease with three major forms: inhalational, cutaneous, and gastrointestinal. Our discussion focuses on inhalational and cutaneous anthrax. Gastrointestinal anthrax is not addressed because this form is unlikely to result from a terrorist attack.


Of the microbes that might be used by terrorists, Bacillus anthracis is among the most dangerous. In October 2001, spores of B. anthracis were mailed to several locations in the United States, causing 22 confirmed or suspected cases of anthrax and 5 deaths. This experience served to heighten concerns regarding the feasibility of terrorist groups using aerosolized bioweapons to stage a large-scale attack.



Microbiology

Bacillus anthracis is an aerobic, gram-positive bacterium. Its name derives from anthrakis, the Greek word for coal (in recognition of the black skin lesions that characterize cutaneous infection). Bacillus anthracis can exist as spores, which are dormant, or as actively growing bacteria. Infection is acquired when the spores enter a host. Ports of entry are skin lesions and the respiratory and GI tracts. In the presence of nutrients (amino acids, nucleotides, glucose), which are abundant in the blood and tissues of the host, the spores germinate and transform into mature bacteria. The mature forms grow and divide rapidly until the nutrient supply is depleted, after which they cease dividing and produce more spores. The mature bacteria cannot survive long outside the host. In contrast, the spores can remain viable in the environment for decades. Anthrax is not transmitted person to person.



Clinical manifestations


Inhalational anthrax.

Infection begins with deposition of anthrax spores in the alveolar space, followed by transport to regional lymph nodes, where germination occurs. Clinical latency can range from 2 days to 6 weeks. Injury results when mature bacilli release toxins, which cause hemorrhage, edema, and necrosis. Once the concentration of toxin has reached a critical level, antibiotics cannot prevent death, even if they kill all circulating bacilli.


Symptoms appear in two stages. Initial symptoms—fever, cough, malaise, and weakness—may be relatively mild. In the second stage, which develops 2 to 3 days later, there is a sudden increase in fever, along with severe respiratory distress, septicemia, hemorrhagic meningitis, and shock. Interestingly, although the infection originates in the lungs, true pneumonia rarely occurs. Even with treatment, the mortality rate can be high: In the U.S. outbreak of 2001, 45% of victims died.



Cutaneous anthrax.

Symptoms begin 1 to 7 days after exposure to anthrax spores. Areas with cuts or abrasions are most vulnerable, but injury can develop at any site where spores land. The initial lesion is a small papule (solid raised area) or vesicle (fluid-filled raised area) associated with localized itching. Within 2 days, the lesion enlarges and evolves into a painless ulcer with a necrotic core. Seven to 10 days after symptom onset, a black eschar (scab-like structure) forms—but then dries, loosens, and sloughs off by day 12 to 14. In most patients, the lesions resolve without complications or scarring. However, if systemic infection develops, the outcome can be fatal. In the absence of antibiotic therapy, about 20% of people with cutaneous anthrax die. In contrast, death among treated patients is rare.



Treatment of established infection

The treatments discussed here reflect consensus-based recommendations published in JAMA in an article titled Anthrax as a Biological Weapon, 2002: Updated Recommendations for Management.



Inhalational anthrax.

Given the rapid course that inhalational anthrax follows, early therapy with antibiotics is essential. Any delay can reduce the chance of survival. Initial IV therapy is preferred to initial oral therapy. However, if there are mass casualties, IV therapy may be impossible, owing to limited supplies and personnel. Ideally, treatment should start with IV ciprofloxacin or IV doxycycline. Because the strain of B. anthracis may be resistant to these drugs, one or two other IV antibiotics should be included. When clinically appropriate, the patient can be switched to oral ciprofloxacin or doxycycline, without additional antibiotics. The duration of treatment—IV plus oral—is 60 days. Specific regimens for adults, children, and pregnant women are presented in Table 110–2 (for limited casualty settings) and Table 110–3 (for mass casualty settings).




Raxibacumab, a monoclonal antibody, represents a new approach to treating inhalational anthrax. Unlike antibiotics, which kill anthrax bacteria, raxibacumab neutralizes deadly anthrax toxins. As a result, the drug can decrease injury even after an infection has become established. Because anthrax infection is rare, raxibacumab has not been tested in humans. However, lifesaving effects have been clearly demonstrated in monkeys exposed to massively lethal doses of anthrax spores. As of April 2009, the manufacturer had supplied 20,000 doses to the U.S. Strategic National Stockpile.



Cutaneous anthrax.

Cutaneous anthrax is treated with oral antibiotics. The preferred drugs are ciprofloxacin and doxycycline. Dosages for adults, children, and pregnant women are the same as those given in Table 110–2 for follow-up oral therapy of inhalational anthrax. Duration of treatment is 60 days. It should be noted that treatment is unlikely to prevent cutaneous lesions, but will prevent systemic complications.



Pre-exposure vaccination

Currently, only one anthrax vaccine—BioThrax (formerly known as Anthrax Vaccine Adsorbed or AVA)—is licensed for use in the United States. BioThrax is an inactivated, cell-free preparation made from an avirulent strain of B. anthracis. The normal immunization schedule calls for three subcutaneous injections given 2 weeks apart, followed by three more injections given at 6, 12, and 18 months. Annual booster shots are recommended thereafter. The most common side effects are muscle and joint aches (20%); headache (20%); local redness, tenderness, or itching (10%); fatigue (10%); nausea (5%); and chills and fever (5%). Serious allergic reactions occur rarely (less than 1 in 100,000).


Who should receive anthrax vaccine? At this time, immunization is limited to people considered at risk. BioThrax is approved only for immunizing (1) people who handle animal products such as hides, hair, or bones that come from anthrax-endemic areas; and (2) people at high risk of exposure to anthrax spores, including veterinarians, laboratory workers, and others whose occupation may involve handling potentially infected animals or other contaminated materials. In addition to these approved uses, BioThrax is being used to vaccinate military personnel. Because the risk of infection in most people is low, routine vaccination of the general population is neither approved nor recommended.



Postexposure prophylaxis: antibiotics plus vaccination

To prevent infection following exposure to aerosolized anthrax spores, the Centers for Disease Control and Prevention (CDC) recommends treatment with an oral antibiotic plus anthrax vaccine. Antibiotic regimens are the same ones employed for treating inhalational anthrax in a mass casualty setting (see Table 110–3). Dosing should start immediately and continue for at least 60 days.


Vaccination following anthrax exposure consists of three doses of BioThrax, given at 0, 2, and 4 weeks. As noted, BioThrax is not currently licensed for postexposure use, or for use in a three-dose regimen. Accordingly, such emergency use would be conducted under an Investigational New Drug application.


New recombinant vaccines are in development. However, when they will be available is uncertain.



Francisella tularensis (tularemia)


Tularemia, also known as “rabbit fever” and “deer fly fever,” is a potentially fatal disease caused by Francisella tularensis, one of the most infectious bacteria known. Inoculation with as few as 10 microbes can cause disease. Infection can be acquired through the skin, mucous membranes, GI tract, or lungs. Terrorists trying to spread tularemia would most likely deliver the bacteria as an aerosol. Tularemia cannot be transmitted person to person.






Yersinia pestis (pneumonic plague)


Plague is a potentially fatal disease caused by Yersinia pestis, a gram-negative bacillus. The disease has two principal forms: bubonic (characterized by tender, enlarged, and inflamed lymph nodes) and pneumonic (characterized by inflammation of the lungs). Bubonic plague is acquired through the bite of a plague-infected flea, and cannot be transmitted person to person. Rarely, an individual with bubonic plague develops secondary pneumonic plague, which can be transmitted person to person (by coughing). Primary pneumonic plague is acquired by inhaling aerosolized Y. pestis. The source of the aerosol could be a person with pneumonic plague, or it could be a biologic weapon. To a would-be bioterrorist, Y. pestis is attractive for several reasons: The microbe is readily available worldwide, culturing large quantities is relatively easy, the bacterium can be aerosolized for wide dissemination, pneumonic plague can be spread person to person, and the fatality rate is high.






Variola virus (smallpox)


Smallpox is a serious, contagious, life-threatening disease caused by the variola virus, a member of the genus Orthopoxvirus. The only natural reservoir for the virus is humans. We have no specific treatment for smallpox, but we can prevent the disease by vaccination, given either before exposure or within a few days after. Because smallpox is highly contagious and because the fatality rate is high (30%), the disease represents a grave threat as a weapon of terrorism.


Thanks to a global vaccination program, endemic smallpox has been eradicated. The last case in the United States occurred in 1949, and the last case on the planet occurred in Somalia in 1977. Because the threat of smallpox had been eliminated, routine vaccination was discontinued—in 1972 for Americans, and by 1982 for the rest of the world.


Ironically, the successful elimination of smallpox has set the stage for its potential return as a weapon of terrorism. That is, if we hadn’t eradicated natural smallpox, then vaccination would still be ongoing. As a result, the population would have immunity, making smallpox useless as a weapon.



Pathogenesis and clinical manifestations

Variola virus enters the body through mucous membranes of the respiratory tract, usually as a result of virus inhalation. Initial exposure is followed by an asymptomatic incubation period (usually 12 to 14 days), followed by the prodromal phase (2 to 4 days), manifesting as high fever, malaise, prostration, headache, and backache. Viral invasion of the oral mucosa and dermis then leads to characteristic eruptions. Small red spots develop in the mouth and on the tongue, and then evolve into sores that break open, releasing large amounts of virus into the mouth and throat. Around this time, a bumpy skin rash develops, starting on the face and then quickly spreading over the entire body. Within 1 to 2 days, the bumps become vesicular (fluid filled), and then pustular (pus filled). About 8 or 9 days after rash onset, the pustules begin to form a crust and then a scab. By 3 weeks after the rash began, the scabs fall off, leaving a characteristic pitted scar.


About 30% of people with smallpox die, usually during the second week of illness. The most likely cause is toxemia associated with circulating immune complexes and soluble variola antigens.

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Jul 24, 2016 | Posted by in NURSING | Comments Off on Potential weapons of biologic, radiologic, and chemical terrorism

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