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Operations Security, Site Security, and Terrorism Incident Response Paul M. Maniscalco Hank T. Christen

• Discuss the definitions of operations security (OPSEC) and site security.

• Describe the difference between OPSEC and site security.

• List the five critical component steps of OPSEC.

• Discuss and describe the intelligence cycle.

• Recognize how OPSEC integrates with the incident command system.

• Discuss the challenges of implementing and sustaining site security.

• Describe the integration of OPSEC and site security for terrorism incident response.

• Recognize the importance of evidence preservation and the role of responders in protecting evidence for law enforcement agencies.

Objectives

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Introduction

When preparing organizations and individuals for re- sponse to a high-impact/high-yield emergency incident, some of the most often overlooked requirements are OPSEC and site security.

Bound inextricably with coordination and integra- tion strategies for response, OPSEC and site security are often compromised in the heat of the battle. Responders, with nothing but the best of intentions, converge on the scene of an incident implementing strategies that, pre-event, have failed to address these most important aspects of the incident response and management strat- egy. The discipline to apply the principles of OPSEC and site security following a preestablished, organized, and well-practiced plan is crucial given the nature of the threat and the variety of conditions that may pre- sent themselves. Failing to address these critical security tenets prior to an event amounts to failing to protect the protectors.

OPSEC

Terrorist attacks present the contemporary emergency response manager or chief officer with more complex challenges and greater probable risks. Site security and OPSEC are multifaceted concepts, bringing together ele- ments ranging from pre-event protection of information concerning an organization’s activities, intentions, or capabilities to operational issues such as scene access, traffic control, and evidence protection. Due to the fact that this involves so many different aspects of disaster response, and because it cannot be completely achieved without full integration of each of those aspects, site security is best understood broadly. Robust control of the incident and proximal areas should be the desired goal. This includes maintaining command and control over the human and material flow into, out of, and around the site, providing for the security and safety of responding personnel, providing these responders with the ability to perform their jobs, ensuring per- sonal accountability and the fulfillment of performance requirements.

For an OPSEC program to be effective, personnel must be aware of OPSEC concerns, implement OPSEC countermeasures when appropriate, and be observant of potential collection activities directed at their orga- nization. This is possible only if the members of the organization understand the range of threats affect- ing their organization and actively support the OPSEC program.

OPSEC Purpose OPSEC as a formalized strategic concept was developed in 1988 under the provisions of National Security Decision Directive 298, The National Operations Security Program. OPSEC is a tool designed to promote operational effec- tiveness by denying adversaries publicly available indica- tors of sensitive activities, capabilities, or intentions. The goal of OPSEC is to control information and observable actions about an organization’s capabilities, limitations, and intentions to prevent or control the exploitation of available information by an adversary. The OPSEC pro- cess involves five steps, which are discussed in greater depth later in this section. These steps are:

1. Identification of critical information 2. Analysis of threats 3. Analysis of vulnerabilities 4. Assessment of risks 5. Application of appropriate countermeasures

The overarching OPSEC framework comences with an assessment of the entire organization/activity in order to determine and identify what exploiable but unclas- sified evidence or classified or sensitive activities could be acquired by an adversary through known collection capabilities—human or technological.

Indication of sensitive activities is often the conse- quence of publicly available information that can be found via a variety of sources including agency Web sites, press briefings, open house events, scheduled exercises, and de- liberate probing of the 911 system by false alarm responses or monitoring daily response actions. This information can then be pieced together to develop critical informa- tion and understanding of agency response tactics, tech- niques, and procedures. Sensitive activities indicators can originate routine administrative, logistics, or operational activities, and if identified, these observations are analyzed via known collection capabilities of an adversary to be employed to exploit vulnerabilities and place responders at risk. An agency chief officer, manager, or safety officer uses this disciplined threat and vulnerability assessment process to determine the current OPSEC state of affairs and guide the agency through the selection and adoption of countermeasures to diminish or eliminate the threat.

OPSEC Process OPSEC considerations must be integral to the process of planning for and integrated with all response doctrine and standard operating procedures (SOP) irrespective of whether they are sensitive operations or not. Similar to the adaptation and adoption of safety principles and engineering controls to keep responders safe, OPSEC tenets should be an integral component of that strategic process.

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Early implementation of OPSEC in the agency response planning process encourages and sustains a heightened awareness by all personnel for maintaining a protective posture for agency-critical information and capabilities. In order to be effective in this arena, the OPSEC planning process requires an unambiguous com- prehension of the specific activity’s mission and agency organizational and operational plans and doctrine. An ef- fective OPSEC program should be seamlessly integrated into an agency’s culture and reinforced by policy, SOPs, and utility in all operational aspects.

The OPSEC planning process must identify and in- corporate strategic/tactical countermeasures, where ap- propriate and feasible, that are necessary to complement physical, information, personnel, signals, computer, and communications security measures. The synergy of the OPSEC system provides an agency with total integra- tion of security countermeasures to blunt vulnerabilities and enhance safety of the responders. An agency might implement OPSEC countermeasures including but not limited to amendment of existing standard operating administrative procedures; application of cover, con- cealment, and deception techniques; and other OPSEC measures that can degrade an adversary’s capability to exploit vulnerabilities. Developing a sustainable and cost-effective security countermeasures program that is tailored to meet the identified threat is one of the central benefits of an agency OPSEC program.

Even though the OPSEC system paradigm is often described as a five-step process, the delineated steps were never intended to be interpreted/implemented as an incre- mental or sequential execution. The program strengths of the OPSEC process are that it is structured to be dynamic and flexible to facilitate an adaptive progression that meets the specific and unique needs of an organization and the operational environment of its jurisdiction. The global strength of the OPSEC process is acknowledged in the final report of the Joint Security Commission where the commission identifies the tenets of OPSEC as the U.S. government’s fundamental basis for risk management.

The five steps of the OPSEC process involve the following:

1. Identification of critical information—Critical information is factual data about an organiza- tion’s intentions, capabilities, and activities that the adversary needs to plan and act effectively to degrade operational effectiveness or place the potential for organizational success at risk. The OPSEC process identifies critical information and determines when that information may cease to be critical in the life cycle of an operation, pro- gram, or activity.

2. Analysis of threats—Threat analysis consists of determining the adversary’s ability to collect, pro- cess, analyze, and use information. The objective of threat analysis is to know as much as possible about each adversary and its ability to target the organization. It is especially important to tailor the adversary threat to the actual activity and, to the extent possible, determine what the adver- sary’s capabilities are with regard to the specific operations of the activity or program.

3. Analysis of vulnerabilities—Vulnerability anal- ysis requires that the OPSEC analyst adopt an adversarial view of the activity requiring protec- tion. The analyst attempts to identify weaknesses or susceptibilities that are exploited by the ad- versary’s collection capabilities. The vulnerabil- ity analysis process must identify the range of activities that can be observed by the adversary, the type of information that can be collected, and the specific organizational weaknesses that the adversary can exploit. Based on this knowledge, the OPSEC analyst determines what critical in- formation the adversary can derive based on the known threat and assessed vulnerabilities.

4. Assessment of risks—Risk assessment is the heart of the OPSEC process. In a risk assessment, threats and vulnerabilities are compared to deter- mine the potential risk posed by adversary intel- ligence collection activities targeting an activity, program, or organization. When the level of vul- nerability is assessed to be high and the adversary threat is evident, then adversary exploitation is expected, and risks are assessed to be high. When the vulnerability is slight, and the adversary’s col- lection ability is rated to be moderate or low, the risk may be determined to be low, and no protective measures are required. Based on the assessed level of risk, cost/benefit measures can be used to compare potential countermeasures in terms of their effectiveness and cost.

5. Application of appropriate countermeasures— In the final step, countermeasures are developed to protect the activity. Ideally, the chosen coun- termeasures eliminate the adversary threat, the vulnerabilities that can be exploited by the adver- sary, or the utility of the information. In assessing countermeasures, the impact of the loss of critical information on organizational effectiveness must be balanced against the cost of implementing corrective measures. Possible countermeasures should include alternatives that may vary in terms of feasibility, cost, and effectiveness. Based on the

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probability of collection, the cost effectiveness of various alternatives and the criticality of the activ- ity countermeasures are selected by the program manager. In some cases, there may be no effective means to protect information because of cost or other factors that make countermeasure imple- mentation impossible. In such cases, the manager must decide to accept the degradation of effective- ness or cancel the activity.

As described, threat analysis is the critical founda- tion of the OPSEC process. Fundamentally, the assessed threat level determines the extent of the agency’s vulner- ability and risk. These findings provide agency leadership with the requisite information to make informed deci- sions relative to mitigating vulnerabilities as well as how to select the most effective countermeasure strategies to achieve the same. Subsequently, it is critical that threat assessment findings truthfully reflect the entirety of the intelligence collection effort that targets the agency.

The Intelligence Cycle

Intelligence is the product resulting from the collection, collation, evaluation, analysis, integration, and interpre- tation of collected information. The intelligence cycle represents an investigation protocol by which informa- tion is acquired, produced, analyzed, and then made available to parties who have a direct need to know or have access based upon specific and definitive agency responsibility (such as the OPSEC officer or fusion center liaison) or operational involvement in a specific matter directly related to this intelligence product. This cycle (FIGURE 7-1) is based upon five distinct functions that gov- ern a critical component of this disciplined process. The five functions are:

1. Planning and direction 2. Collection

3. Processing 4. Production 5. Dissemination

Each segment of the intelligence cycle has a spe- cifically crafted function that provides valuable contri- butions to the end product of the entire process. The functions are described as follows:

1. Planning and direction—This step involves the management of the entire intelligence effort, from the identification of a need for data to the final delivery of the intelligence product to the consumer. The process consists of identifying, prioritizing, and validating intelligence require- ments; translating requirements into observables; preparing collection plans; issuing requests for information collection, production, and dissemi- nation; and continuously monitoring the avail- ability of collected data. In this step, specific collection capabilities are tasked based on the type of information required, the susceptibility of the targeted activity to various types of collection activity, and the availability of collection assets.

2. Collection—This step includes both acquiring information and provisioning that information to processing and production elements. The col- lection process encompasses the management of various activities, including developing collection guidelines that ensure optimal use of available intelligence resources. Intelligence collection re- quirements are developed to meet the needs of potential consumers. Based upon identified intel- ligence, requirements collection activities are given specific tasks to collect information. These tasks are generally redundant and may use a number of different intelligence disciplines for collec- tion activities. Task redundancy compensates for the potential loss or failure of a collection asset. It ensures that the failure of a collection asset is compensated for by duplicate or different assets capable of answering the collection need. The use of different types of collection systems contributes to redundancy. It also allows the collection of dif- ferent types of information that can be used to con- firm or disprove potential assessments. Collection operations depend on secure, rapid, redundant, and reliable communications to allow for data exchange and to provide opportunities for cross- cueing of assets and tip-off exchanges between as- sets. Once collected, information is correlated and forwarded for processing and production.

3. Processing—This step involves the conversion of collected information into a form suitable for FIGURE 7-1 Intelligence cycle.

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the production of intelligence. In this process, incoming information is converted into formats that can be readily used by intelligence analysts in producing intelligence. Processing includes such activities as translation and reduction of intercepted messages into written format to per- mit detailed analysis and comparison with other information. Other types of processing include video production, photographic processing, and correlation of information collected by technical intelligence platforms.

4. Production—This step is the process of analyz- ing, evaluating, interpreting, and integrating raw data and information into finished intelligence products for known or anticipated purposes and applications. The product may be developed from a single source or from collection and databases. To be effective, intelligence production must fo- cus on the consumer’s needs. It should be ob- jective, timely, and most importantly accurate. As part of the production process, the analyst must eliminate information that is redundant, erroneous, or inapplicable to the intelligence re- quirement. As a result of the analytical effort, the analyst may determine that additional collection operations are required to fill in gaps left by previ- ous collection or existing intelligence databases. The final intelligence product must provide the consumer with an understanding of the subject area and draw analytical conclusions supported by available data.

5. Dissemination—This step is the conveyance of intelligence to the consumer in a usable form. Intelligence can be provided to the consumer in a wide range of formats including verbal reports, written reports, imagery products, and intelli- gence databases. Dissemination can be accom- plished through physical exchanges of data and through interconnected data and communica- tions networks.

An agency OPSEC manager must be familiar with the intelligence cycle for three essential reasons. First, awareness allows the OPSEC manager to assume a role in the required intelligence production to effectively support the agency OPSEC initiative. OPSEC managers must be acutely aware of the range of threats confronting the agency to ensure they implement effective counter- measures that deny adversaries access to data that pro- vide critical information.

Next, comprehension of the intelligence cycle and associated functions provides the agency OPSEC manager with the critical insight and threat perspec-

tive to develop protective measures in order to thwart adversary collection activities that could undermine re- sponse effectiveness and responder safety. The OPSEC manager’s knowledge of an adversary’s collection methods and patterns allows the program manager to develop effective countermeasures that hide or distort indicators that could be used against the agency and its personnel.

Lastly, knowledge of the adversary’s analytical bi- ases is used to develop deception programs that deceive the adversary by confirming erroneous perceptions. For example, expectations that agency credentials are ex- ploitable to the point of personnel counterfeiting IDs, be- lieving that official vehicles can be stolen from vendors, or that uniform articles can be acquired without proper credentials allow the adversary to exploit the public’s trust and confidence in an agency by masquerading as responders to launch an attack.

The importance of a coherent and seamlessly in- tegrated OPSEC program in the contemporary public safety and emergency response agencies’ SOPs cannot be overstated. In the changing world, where emergency re- sponders are no longer viewed as noncombatants and are being targeted as part of the larger terrorist plot, adoption and implementation of a robust, integrated OPSEC pro- gram is an obligation, not a luxury. Organizations such as the International Association of Emergency Medical Services Chiefs (IAEMSC), International Association of Fire Chiefs, and the International Association of Chiefs of Police all have OPSEC and operations site security best practice reference documents that one can access and use when crafting one’s own agency protocols. An example of the reference sheet from the IAEMSC is listed herein for review (FIGURE 7-2).

This chapter segment does not presume to present an exhaustive, comprehensive representation of intel- ligence processes and OPSEC processes; however, it does provide the learner with the opportunity to de- velop a fundamental, analytical, historical, and theoreti- cal understanding for further research on the general subject of intelligence and OPSEC. Learners are encour- aged to discuss these issues in greater detail with their intelligence officer liaisons and local/regional fusion center representatives. Additionally, information and training on OPSEC can be obtained through a variety of sources, including the Federal Law Enforcement Training Center and the Interagency OPSEC Support Staff at www.ioss.gov, or IOSS, 6411 Ivy Lane, Suite 400, Greenbelt, MD 20770; (443) 479-4677.

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FIGURE 7-2 IAEMSC-recommended EMS agency operational security measures.

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FIGURE 7-2 (Continued)

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FIGURE 7-2 (Continued)

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Incident Management/Unified Command as the Foundation for Safety and Security

The framework that makes for effective and successful deployment of OPSEC and site security strategies is the incident management/unified command (IM/UC) struc- ture as articulated in the National Response Framework (NRF) and the National Incident Management System (NIMS). Many OPSEC and site security issues are ad- dressed by properly applying these disciplined and stan- dard structures, practices, and protocols. For example, interagency integration problems involving the establish- ment of a chain of command, which produced many of the issues that plagued security at the World Trade Center site in the aftermath of the September 11, 2001, terrorist attacks, could have been significantly amelio- rated by the implementation of an effective IM/UC early in the incident and the immediate establishment of a workable security perimeter.

Simply restating the requirement for implementing the IM/UC system, which has already been established with the release of the NRF and the resulting NIMS, is not the purpose here. Moreover, this chapter section seeks to address the issue of the role OPSEC and site se- curity plays in the response to a terrorist incident within the framework of the IM/UC process.

Although it is in the blood of every individual who chooses to devote his or her life’s work to respond- ing when others are fleeing, we must resist the urge to run in without fully understanding what we face beyond a door, on the other side of a cloud of smoke, or around a corner. Although this is easier said than accomplished, in a terrorist event, our survival to fight another day depends on projecting or knowing what threats lie ahead.

The organizational protocol that is established by IM/UC is simply the framework by which OPSEC/site security is efficiently, effectively, and successfully es- tablished; in other words, it is required but not self- sufficient. While not a panacea, IM/UC implementation is crucial for us to remediate the hard lessons learned in the recent past, fixing the strategic and operational problems inherent in past responses and implementing standards for OPSEC and site security.

The adoption and implementation of the NIMS–IM/ UC framework addresses and corrects a large por- tion of site security issues by the talents and service provided via the law enforcement community at the command post. It is important to note, however, that not all of these issues are terrorism specific, and the UC concept should be allied at most emergency scenes.

Many of the difficulties inherent in the massive re- sponse of multiple agencies are as prevalent in an earth- quake as in a dirty bomb attack. What makes the issue of OPSEC/site security so important and unique in the context of terrorism is the particular nature of the threat. The unpredictability of terrorism creates conditions that are fluid, requiring speed and flexibility of thought and action as well as thorough planning and preparation. Furthermore, the targeting of responders and “soft tar- gets” such as healthcare facilities and schools makes this an even more complex matter to address and manage to ensure one’s safety and the safety of those responders who are being coordinated at the scene.

In analyzing many major recent terrorist attacks, numerous areas of concern consistently emerge. By iden- tifying each of these and focusing on the pitfalls of the response at the time, as well as stating how the response could have been improved, responders can learn lessons and establish best practices for future incidents. These concerns fall into two general categories. The first cat- egory involves those concerns that are potentially pres- ent in any sort of disaster and that are remedied by the proper implementation of IM/UC. These include:

• Victim rescue in the immediate aftermath of an incident

• Personnel needs including work shifts to en- sure proper rest, adequate personal protective equipment, and continuation of normal EMS/ law enforcement/fire services over the course of the event

• Organizational integration/interoperability communication issues

• Public relations, including providing informa- tion to dignitaries, media, charities, and fami- lies of victims/missing

• OPSEC/site security • Staffing support for other elements The second category of concern addresses those

concerns unique to terrorism that cannot be addressed simply by the implementation of IM/UC, thereby requir- ing further attention and creativity. These include:

• Search for secondary devices and hostile threats to the scene and responders

• Perimeter establishment and access control • Traffic and crowd control • Evidence recovery and protection

OPSEC/Site Security—Challenges of a General Nature The importance IM/UC plays in enabling successful OPSEC/site security cannot be overstated. Perhaps the key component in OPSEC/site security is communication

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and coordination among responders, and the primary fo- cus of IM/UC is just that. The following section addresses each aspect of OPSEC/site security that is helped by the implementation of IM/UC, including multiple examples from recent terrorist attacks where such implementation resulted in saved lives or property, and suggestions on implementing site security at future incidents or events.

Victim Rescue

The first challenge to OPSEC/site security is victim res- cue in the immediate aftermath of an incident (FIGURE 7-3). This is the initial and most dramatic problem faced by all responders during and immediately following a terrorist attack. As mentioned briefly before, a driving characteristic that defines all responders is the natu- ral instinct to rush forward, nobly doing whatever one can to quickly save as many lives as possible. For the safety of the responders and the victims, some restraint and organization must be exercised, or the overall in- cident outcome may become negative, and people may die needlessly. The lasting images from the events of September 11, 2001, are of the hundreds of first re- sponder personnel rushing to the scene to help all who were victimized by these horrible attacks. One striking example in a day full of actions hampering, hindering, and preventing all good intentions was the Shanksville, Pennsylvania, plane crash site, which on September 11, 2001, was overwhelmed and severely congested due to the phenomenon of response units, both on and off duty,

making their way to the scene either by self-dispatch or by convincing dispatchers to send more help. The resulting chaos clogged the scene, severely complicat- ing command and control, and confusing perimeter maintenance. Additionally, similar conditions emerged in New York City after the mayor announced on televi- sion that all available resources should be brought to bear at the World Trade Center site. This resulted in numerous well-meaning individuals self-dispatching to the scene, creating an incredible problem with respect to validation of personnel claiming to possess certain capabilities, skills, certifications, and licenses, as well as personal accountability for those operating on the scene during the initial days postevent.

This area of OPSEC/site security primarily deals with ensuring an effective response rather than an unorga- nized, potentially dangerous, and surely less effective response. Implementation of IM/UC could have dimin- ished the reported congestion and ensuing confusion at both events because it states that off-duty response per- sonnel should not respond to an incident unless directed to do so. Although operational doctrine dictates that you man your post until otherwise directed, the reality is that such a situation rarely exists. The instinct to respond is powerful and is complicated by the “touch the plane” phenomenon, in which people feel they have to be at the disaster scene so they can tell others that they were there when it happened. Therefore, it is incumbent on the agency and organization leaders to stress and practice operational discipline that demands coordination and adherence to strict deployment protocol.

Another relevant example is the Bali bombing of October, 2002. As with all responders, the Bali respond- ers rushed in to help victims and save as many lives as possible. However, OPSEC/site security was nonexistent, and many more lives were in danger in the event of coordinated secondary attack. Though it is difficult to find fault with the selfless actions of such responders, it is crucial that this emotional response be tempered by reason and the knowledge that restraint and discipline are not only necessary, but required to keep responders safe and ensure that the investigation is not fouled by re- sponder crime scene contamination thwarting attempts to bring the perpetrators to justice.

Finally, there is the example of the brave responders to the World Trade Center attacks. In their zeal to charge into the scene and save as many people as possible, the tunnel vision they experienced most likely contributed to an ineffective assessment of the prevailing danger and catastrophic structural failure of the towers. This is a tremendously unique incident in our history with no historical reference point, and the multiple planes em-

FIGURE 7-3 Victim rescue is an initial objective and a key problem faced by all responders during and after a terrorist attack.

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ployed in the attack were effective secondary devices of significant proportion.

OPSEC/site security involves understanding the situation to the greatest degree of accuracy possible, including the possibility that attempting to rescue vic- tims immediately may not be the wisest, safest, or most appropriate course of action. Though it may seem that delaying rescue efforts is tantamount to abandonment of our duty to act and is contrary to the oath many of us swear to, in the end, lives may be saved by taking the time to fully assess the situation in a coherent fashion prior to operational response execution.

Personnel Needs The security needs of response personnel are a major issue to be addressed in planning for response to a high- impact/high-yield emergency incident. The needs are varied and complex, complicated, and resource demand- ing during and after a terrorist event. These demands are further amplified given the dual threat of the likelihood of hazardous materials being present and the active in- tent of the terrorist(s) to hurt or kill as many people as possible, including responders.

One good example of personnel needs was the 1997 sarin attacks in the Tokyo subway. Japanese medical personnel lacked proper personal protective equipment; more than 20% of the staff of St. Luke’s International Hospital exhibited some sort of detrimental physical ef- fects after treating victims of the attack. Had the hospital planned properly and equipped the facility/personnel, in addition to regularly training all employees, the in- stances of secondary contamination would have been greatly reduced.

The most recent and well-known example of re- sponders lacking proper personal protective equipment was the September 11, 2001, attacks. Early on in the re- sponse, heavy particulate asbestos and other hazardous materials contaminants, including Freon and cadmium, were found at the site, yet there were responders with- out proper protective equipment. This was attributed to both poor planning and logistics acquisition prob- lems, because there was simply not enough equipment to go around—indicating that planners failed to grasp the scope or even believe that an attack of that magni- tude could occur—and on poor logistics management, because some of the needed equipment was present (on- scene) but was not distributed properly.

There is another critical aspect to protecting re- sponders in a traditional sense; personnel rest and re- habilitation are critical to the success and sustainability of an operation. Although responders are often willing to work to the point of exhaustion, doing so is danger-

ous to the responders, the victims, and the effectiveness of the operation. Fatigue creates more victims through poor decision making, increased stress, frustration, and impaired judgment. The medical profession continues to address the effects of sleep deprivation and fatigue due to errors directly traced back to exhausted healthcare providers. Several well-publicized studies that chronicle the effects of long work hours in life-and-death, stressful environments reveal that errors have produced increased morbidity and mortality in the patients being cared for by these well-meaning professionals. Studies conducted over the last several years reveal that moderate sleep deprivation produces impairments in cognitive and mo- tor performance equivalent to illegal levels of alcohol intoxication.

The last thing any coordinated response should have to deal with is victims among the responding rescue workers. To help prevent and ensure the equitable and safe distribution of personnel, IM/UC has instituted a system by which the incident commander assigns shifts to the workers, thereby forcing rest on the weary, whether they realize they need it at the time or not. The final personnel issue to be addressed is the continuation of public services, including EMS, medical, law enforce- ment, and fire service, through the end of the incident and into the recovery and mitigation stages.

Sustaining 911 response capacities for the entire community must be a significant goal that all agencies strive to achieve. Just because the agency is confronted with a large disaster in the community does not allevi- ate it from the obligation to ensure the best possible planning efforts to at least attempt to provide appropri- ate management of all emergencies in the community. Clearly the fiscal implications of having a sustainable and robust response system that can handle any and all 911 calls at all times are strictly cost prohibitive. The burden sharing that has become widely accepted is the use of mutual aid compacts between communities, regions, and now states under the Emergency Management Assistance Compact. The key to sustained successful operation is embracing this concept and employing it on a regular basis. Further, a review of response protocols for uni- formity, ensuring interoperability, and having a shared vision of application of OPSEC and site security tactics are integral on “game day.”

Hospitals share the same concerns for their facili- ties and staff. During the planning phase for respond- ing to disasters, hospital planners must take the time to consider a number of issues that previously did not require their attention. Such matters include increased security, physical management of patient flow, personal protective equipment, decontamination strategies, staff

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training, and personnel support. One such hospital fail- ure that resulted in much national media attention oc- curred in Florida during the hurricane season of 2004. In this case, Florida Hospital-Ormond Memorial fired or suspended about 25 nurses for not working during Hurricane Frances. Some nurses were fired for not call- ing in, not showing up, or refusing to work, while others were suspended for not completing a shift. The hospital stated that under hospital policy, critical care employees are required to work during a disaster. Some nurses responded in media accounts alleging that they were not trained to deal with these extreme scenarios and also questioned who would protect their families. No matter the reason, staffing rosters that were expected to be populated based upon the internal disaster plan were not, leaving the facility in a lurch to cover staff vacancies and sustain operations.

Another unfortunate occurrence in the aftermath of disasters is civil unrest and criminal activity. Police presence is often distracted and concentrated at the site of the disaster, coverage is weakened in the areas where law enforcement officers would normally patrol or de- ploy, and if the presence is weakened enough, citizens might loot nearby houses, commercial districts, and in some cases emergency response equipment. Examples of this were found during and after countless disasters, including Hurricane Charley’s landfall in Florida, and there were unsubstantiated accusations of looting by the responders themselves in the September 11, 2001, at- tacks on New York City. In 2005, after Hurricane Katrina hit New Orleans, there was considerable media attention on allegations of emergency responder and law enforce- ment involvement in looting. In 2009, there were still grand jury investigations regarding numerous allegations that were leveled at responders ranging from thefts to abuse of authority and civil rights violations.

Community planners, responders, and emergency services personnel must also consider the likelihood of a situation where events have created a large scale area that is too dangerous for anyone to enter or in which to respond. Responders must ask themselves two questions—and answer honestly. (1) In such a given situation, what are the primary responsibilities of responders in getting people out, keeping people from entering, and making sure that the area remains contained? (2) Are we currently prepared to evacu- ate, relocate, secure, and effectively close a significant portion of or an entire city as was necessary during the 1986 Chernobyl nuclear power plant disaster or Hurricane Katrina?

Proper and effective deployment of law enforce- ment officers is a key aspect of incident management,

NIMS, and the NRF. With proper law enforcement tactical implementation, the lion’s share of criminal activity or any form of civil disorder can be mitigated. The implementation strategy also provides for more ef- fective coordination of responders at the scene, afford- ing a higher level of coherence to ensure that security of all personnel, integrated operations, investigatory processes, and sustained evidentiary recovery can be achieved.

A similar concern exists for fire services in the wake of a disaster, specifically in fire-heavy disasters. The typi- cal response for the fire service is to rush to the scene of a major blaze, such as the World Trade Center, and engage as quickly as possible to control the threat and resolve the problem. One can only imagine the collateral dan- gers if coincidental fires emerge in other parts of a city, particularly in the event of a secondary terrorist attack. The successes of mutual aid are clearly evident in the various responses to a number of large-scale disasters, but especially on September 11, 2001.

Emergency management professionals often speak of the secondary attack. How many communities, agen- cies, and/or organizations responsible for response and recovery actually have plans in place for a controlled, co- ordinated, organized deployment in the face of a growing disaster? Can the existing response plans and operational doctrine withstand a campaign event challenge?

Despite what most would believe, and as horrible as the September 11, 2001, attacks were, the United States has yet to experience a true mass casualty, mass fatality event that overwhelms the capabilities of the affected community and the country. As emergency responders and leaders, we must revisit the pain and shock we all felt on September 11, 2001, when almost 3,000 people were murdered. Three thousand sounds like an unimaginable number, but to our enemies, based upon their stated intent to inflict harm, 3,000 is a training exercise.

Integration Integration issues are a central consideration in any emergency response, but they are critical for a large- scale incident. The most obvious example of this is in the immediate aftermath of the September 11, 2001, attacks on the World Trade Center in New York City. Lack of interoperability between fire and police radios was found to be a major problem during the response to the 1993 bombing of the World Trade Center, and unfortunately, the same problem reared its ugly head on September 11, 2001. Due to this failure and overloaded radio equipment, fire fighters in World Trade Center tower 1 were unaware of reports of the imminent col-

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lapse of the tower from a New York Police Department (NYPD) helicopter and therefore did not initiate their own evacuation. This lack of communication resulted in an increased number of casualties that might have been avoided. The proper implementation of IM/UC, which stresses both horizontal and vertical information sharing, would have required interoperable radios, and the NYPD helicopter in the air above the World Trade Center would have been able to relay the information regarding the collapse directly to the fire department, allowing fire fighters to have a fuller depth of under- standing for the events and begin evacuating.

The Moscow theater siege of October 2002 is an- other tragic example of the cost of lives lost when agen- cies are not integrated. Chechen terrorists took over the theater, claimed the patrons as hostages, and were killed when Russian commandos pumped a toxic gas into the theater, which rendered both terrorists and hostages unconscious, in some cases killing them. The refusal and delay by Russian authorities to release information regarding the type of gas used to subdue and incapaci- tate the Chechen terrorists rendered medical personnel unable to properly diagnose and treat the nearly 650 hostage victims of the gas, 117 of whom perished in the rescue. The unfortunate reality is that authorities in the Spetsnaz (Russian Special Forces, who carried out the raid) did not involve the medical community or on- site medical responders. If the Spetsnaz had coordinated the assault and included a medical component in tacti- cal operations, the critical medical communication and coordination would have positioned the rescue attempt for greater success, saving additional lives because the medical knowledge, treatment, and response capabili- ties would have been on scene and poised to effectively intervene when called upon.

The Press and Dignitaries

Public relations is an important aspect of OPSEC/site security because outside factors such as the media and the victims’ families can seriously complicate a response or errantly alter public understanding and perception of the response actions and effectiveness. An example of the lack of OPSEC/site security with respect to the media causing major problems was evident during the Beltway sniper shootings of October 2002. The sniper pair left notes for the police with specific instructions not to be relayed to the press, and allegedly made numerous re- quests for the media not to be involved in the interaction between the sniper and police. The press obtained this information through the notorious unnamed source and

went public with information that not only jeopardized the investigation, but also put many lives in danger. The resulting lack of trust between the snipers and the po- lice impeded communication between investigators and the perpetrators, slowing the investigation as authorities shifted focus toward damage control.

The media is a valuable asset when responding to an incident, provided relations take place in a controlled, efficient manner. An example of the positive and negative role the media can play in responding to an event was during the sarin attacks in Tokyo. The most common and frustrating problem during any response is a lack of information and communication. In the Tokyo incident, personnel at local hospitals had no idea what type of haz- ardous material or contaminant was creating their medical problems. The hospital personnel dealing with the un- known became aware of the substance from watching the local television broadcasts. Coincidently, physicians who had experience with sarin and the effects on humans were also watching. The resultant communication between the physicians viewing the news coverage and the hospitals correctly identified the culprit substance. Concurrently, the media was criticized for filming while people suffered and died instead of helping them to the hospital.

Media coverage of terrorist events can be a double- edged sword, and it is up to planners to ensure that the benefits of having the media present are not outweighed by the disadvantages. This entails having a public infor- mation officer (PIO) who is trained prior to an incident on the successful discharge of the PIO duties that are integrated into the command structure to assist with response information dissemination and management of the media (FIGURE 7-4). The PIO must work closely

FIGURE 7-4 The public information officer is trained prior to an incident on the successful discharge of the PIO duties integrated into the command structure and can therefore assist with response information dissemina- tion and management of the media.

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with the OPSEC officer to determine what information is shared with the media so that the released information does not compromise the integrity of the investigation or the safety of responders operating at the scene.

In the event of a major disaster, it is common prac- tice for government officials of all levels to visit the site to offer reassurance, including governors visiting the areas devastated by disaster in their states and the president coming to the scene of a disaster to lend support and wit- ness the operations in person, such as after September 11, 2001. It is necessary to have strict OPSEC/site security to maintain the safety of these dignitaries. Concurrently, OPSEC/site security is also structured to ensure the dig- nitaries or their entourages do not disrupt operations, disturb the scene, or hinder investigations. While the visit of these dignitaries is important to reassure the pub- lic, it must not come at the cost of successfully executing the local or state recovery efforts or the strategies in the NRF. As has been stated, planning cannot take place in a vacuum; plans to deal with the onslaught of media and dignitaries must be a part of the ongoing community response to any event that may overwhelm a commu- nity’s ability to operate under normal daily conditions. Therefore, meet, greet, and planning meetings must be conducted with all involved parties to include the lo- cal media representatives with the primary goal that all participants have a job to do and planning prior to the worst case scenario will allow for the completion of the mission in a safe and cooperative manner. All egos, pre- conceived assumptions, and negative relationships must be checked at the door.

OPSEC/Site Security Demands for Off-Site Operations

OPSEC personnel must also take into account the issue of security and staffing support for elements of the re- sponse not located directly at the event site, such as joint or regional operation centers, joint or regional informa- tion centers, multiagency coordination centers, morgues, food distribution, and donation reception sites. While these sites may not be physically located inside the inci- dent perimeter, they are likely targets. These critical ar- eas are vulnerable to being compromised or attacked by a variety of means including, but not limited to physical attacks with arms, explosives, criminal acts, and hazard- ous material dispersal.

Law enforcement officials, such as federal marshals or local police or security forces, must be present to ensure protection and sustained operation of these vital services. It is vital to the success and continuation of

the response that community planners, local, city, and county emergency managers and responders (career and volunteer) meet on a regular basis prior to a catastrophic emergency to promulgate prudent operational response doctrine, to ensure OPSEC and site security, and lastly to test planning strategies through comprehensive robust exercising activities.

OPSEC/Site Security for a Terrorist Incident

It isn’t enough simply to adopt and fully implement the NIMS–IM/UC framework in order to control and overcome the majority of OPSEC/site security issues, although it is important to note that the majority of con- cerns, challenges, and problems faced by EMS, medical personnel, law enforcement, security personnel, and fire service are not unique to terrorism/weapons of mass de- struction events. The implementation of a plan and/or a system to alleviate identified problems and to avoid new problems is only as good as the training that is provided to familiarize all those who will utilize the plan and/or system. It is impossible and may border on negligence to expect that people, agencies, departments, and com- munities will be able to utilize plans designed to place everyone on the same sheet of paper without coherent and comprehensive ongoing training and exercising.

In the case of a natural disaster, for example, the difficulties inherent in the massive response of multiple agencies remain. The logistics involved in mobilizing personnel, equipment, and resources coupled with emo- tions, hungry, tired victims, and those nefarious few who are bent on taking advantage of victims in need creates circumstances that will derail the best laid plans. Now, add to that a situation where these very same people are asked to respond, faced with all the normal obstacles, but have had little or no time to be acquainted with the new plan and even less time being trained on the plan’s usefulness, purpose, and operational guidance. You now have the current scenario in place; add to this already chaotic, stressful, and incredibly frustrating event the current severity and the particular nature of the threats we face in the post–September 11, 2001, era.

The unpredictability of terrorism presents condi- tions that are highly fluid and subject not only to the whims of nature or the physics of a damaged building but to the advanced plans and suicidal determination of well-trained terrorists. Additionally, a garden variety ter- rorist does not abide by Occupational Safety and Health Administration requirements, does not apply for permits, does not worry about the adequacy of financial support, does not follow labor laws and/or legal restraints pre-

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venting action, and the list goes on and on. The terrorist groups that have been identified, and most likely those we have yet to uncover, commit, plan, train, and act in an organized, efficient, and effective manner.

An organizational structure adequate to deal with such an elusive threat, represented by NIMS–IM/UC, only provides the means by which proper measures can be successfully implemented. This is not a ques- tion of whether a strategy will be properly followed, but what the strategy entails. The plan in no way pro- vides implementation funding, training and educational funding, staffing backfill, or overtime funding, allowing comprehensive training and education, equipment ac- quisition, and maintenance. Any plan is only as good as the assumptions it is based on, and a plan certainly is useless when those utilizing the plan have yet to see the plan, be familiar with it, and receive training in plan implementation.

The critical issue is the priority that must be given to OPSEC/site security at all incidents, not just those eventually identified as terrorism related. Adoption of this position creates a familiarity with OPSEC and site security for all responders and becomes institutional- ized into the way we do business 24 hours a day, 7 days a week.

The after action reports from numerous major ter- rorism incidents clearly reveal shortcomings in OPSEC/ site security that warrant significant emphasis and close attention by agencies developing their terrorism/WMD response plans in concurrence with NIMS–IM/UC.

There is a striking convergence of properties that characterizes this second group of OPSEC/site security concerns: that they cannot be solved by organizational reform alone, and that they are all particularly pertinent in a terrorist attack. This highly interconnected list for scene management includes perimeter establishment, access and egress control, personal accountability, evi- dence protection and chain of custody, and the search for secondary devices and threats. Solving the inadequacies in these areas requires not just that the organizational structure exists, but that it be imbedded in a prominent position within the incident command structure.

Establishing a Perimeter

The effective establishment of a perimeter is often a cru- cial aspect of gaining control over the scene of an attack. Establishing a perimeter has ramifications in all aspects of maintaining OPSEC/site security. Force protection cannot be assured, evidence cannot be protected, chain of custody cannot be guaranteed, and access to the scene

cannot be controlled with a porous or haphazard cre- ation of a perimeter.

The overall response to the 1995 terrorist bombing of the Alfred P. Murrah Federal Building in Oklahoma City, Oklahoma, is an excellent model of what was right and what was wrong. There were three layers of perimeters quickly established by morning on the day after the bombing; the inner perimeter was designed to provide limited access to only those personnel autho- rized to participate in the rescue/recovery work and the criminal investigation, a staging area that also served as a buffer for workers, and a limited traffic access cordon. Unfortunately, an effective perimeter was not established immediately and the site quickly became overwhelmed with hundreds of well-meaning people who wanted to help in any way they could. The problem was that no control existed over any area of the dangerous site and one convergent responder—a nurse—was killed early on due to falling debris.

The eventual establishment of an effective perimeter was accomplished by close coordination of disparate agencies and proper utilization of their abilities along with the securing and construction of fencing. At the World Trade Center site on September 11, 2001, in admittedly more trying circumstances, “Perimeter se- curity was not adequately established, allowing large numbers of unnecessary personnel to enter” (McKinsey & Company) due in large part to a 5-day delay in the creation of an adequate credentialing system and the construction of a fence. It took an extra 4 days at the World Trade Center to establish security even approaching the perimeter set up at the Murrah Federal Building. The potential repercussions for this sort of inattention are massive.

Another example of the need for perimeter secu- rity is the case of a 1997 bombing of a women’s clinic in suburban Atlanta, where Eric Rudolph is alleged to have planted a secondary explosive device timed to detonate upon the arrival of personnel responding to the initial explosive event. A CNN camera crew filming an interview with a witness of the initial blast caught the nearby second explosion on film; both media and civilians were endangered because they were allowed access to an area surrounding the scene, which should have been secured.

The uncontrolled scene increases the potential and likelihood that individuals not involved in the initial catastrophic event will become victims as a result of a secondary attack, the hazardous material (if present) will be spread to a wider area, and the criminal investigation will be hampered or evidence destroyed. Ground zero at a terrorist attack, therefore, demands special attention to

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the formation of perimeters as a necessary prerequisite to full OPSEC/site security implementation.

The cooperation and discipline required to ensure security and safety does not and will not happen over- night or because it is the right thing to do. All aspects of scene control must be carefully planned, practiced, and exercised on an ongoing basis. It is impossible to expect two completely divergent disciplines to come together and cooperate without the right training and education. A vital perspective to understand in this matter is the doctrinal conflict that this creates—attribution versus intervention. One large group of responders is running in to tear the scene apart to look for victims and survivors and to treat the injured (intervention). The other large response group requires the meticulous preservation of evidence and maintaining the site just as it was found (attribution).

There is no question that each group has a vital and important role and responsibility—none more im- portant than the other. It is naïve and irresponsible for any responding person, agency, group, or department to expect these two parallel forces to eventually meet in the middle without long-term focused efforts aimed at settling the differences and ensuring that both jobs are completed efficiently and timely. A mutual respect must be achieved through policy and reinforced through exercising if the contemporary emergency response and public safety professions realistically expect to bridge the intervention–attribution gap. This can only be ac- complished well before the incident response through regular meetings, educational sessions, training, and ef- fective exercising opportunities. Failure to address this coordination factor pre-event will result in a response that resembles a cacophony—not the desired symphony.

Scene Evidence Preservation As previously stated, ensuring the preservation of evi- dence is another fundamental aspect of OPSEC/site se- curity in the event of a terrorist attack. Consider the Oklahoma Department of Civil Emergency Management after action report, which outlines the problems that presented themselves because of the large number of volunteers who were incorporated into rescue operations without being registered or identified. “Since the site was a crime scene, all our volunteers were required to be critically screened before they could work at the bomb site” (Oklahoma Department of Civil Emergency).

Fortunately, authorities implemented this system to rectify the unimpeded access people were afforded; about 30 unauthorized convergent responder volun- teers were evicted from one floor alone. This was not handled as well at the site of the 2002 Bali bombings.

There, “the crime scene was seemingly ruined and un- protected” (Pastika) due, in addition to unavoidable cir- cumstances involved in the response, to “the public’s curiosity,” (Pastika) which was apparently allowed to hinder the investigation despite the fact that a police line had been set up.

The removal, addition, destruction, or alteration of material, whether intentional, unintentional, or sim- ply the product of an inexperienced volunteer seeking a souvenir, could be a major hindrance to the proper conduct of the criminal investigation and identification of those responsible. Even the most minute and seem- ingly unimportant pieces of evidence often prove to be irreplaceable in these situations, and they cannot afford to be compromised. To the untrained eye, the aftermath of a terrorist attack is a pile of debris or a chaotic mass of humanity. To the trained criminal investigator, the scene is a roadmap that tells the complete story of the circum- stances leading up to the event and the event itself. As noted previously, the control of access to the site of a terrorist incident through well-guarded and protected perimeters and a secure credentialing system that does not allow for forgeries is the only way to guarantee the integrity of the crime scene.

The Influence of Traffic and Crowd Control upon an Incident Scene Traffic and crowd control make up an extremely impor- tant aspect of scene OPSEC/site security, especially in the wake of a terrorist attack. With this aspect, OPSEC/ site security takes on a much broader impact subse- quent to the flow of people and materials in and out of the site itself, and the city or general area in which the attack has occurred is impacted by activity elsewhere. The frightening nature of terrorism, especially for cases in which chemical, biological, radiological, or nuclear (CBRN) substances are implicated either by fact or by speculation, could result in mass hysteria and chaos. In the absence of accurate, timely information from au- thorities, rumor mongering can take root, leading to potentially disastrous public panic. Something in the vein of an uncontrolled, large-scale attempt to flee a city in the midst of reports of a CBRN incident could freeze attempts to contain the attack or worse, prompt more people into the affected area, and risk exposure to a greater slice of the population.

Consider the description of the evacuation of coastal Florida at the approach of Hurricane Floyd in 1999: “Even many of those not in evacuation zones fled at the sight of satellite images on the news, which depicted a monstrous Floyd larger than the entire state of Florida … the result was a transportation nightmare” (Kriner).

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The Florida public, frightened by memories of 1992’s Hurricane Andrew, is akin to today’s nationwide mem- ory of September 11, 2001; combined with sensational- izing factors such as talk of a hurricane engulfing a state or the imminent citywide release of a chemical agent, they can easily produce wholesale disorder. Full control of the site of a terrorist incident area requires that the information being disseminated from a scene be released in multiple media and methods of communication to dispel rumors, with an eye to directing the public to the proper course of action. Emergency response managers and chief officers cannot lose sight of the fact that our communities are made up of cultures that interpret the same information in different ways. Keeping in mind the cultural, language, and educational barriers that make up each community requires extensive preparations to ensure a complete information sharing plan of action. Concurrently, traffic and crowd control of the entire surrounding area must be fused with information con- trol to ensure that on-site efforts receive proper support and aid.

Control of human traffic also has great importance in its localized form. In the rush to leave a scene to avoid injury or seek medical attention, it is very possible that citizens will unintentionally carry hazardous substances, particularly CBRN material, with them. Depending on the nature of the agent that has been introduced, the failure to contain contaminated people or other material could lead to secondary contamination of individuals or property.

The 1995 sarin nerve agent attack on the Tokyo sub- way system is an example of the difficulties and effects associated with the uncontrolled vector of contaminated victims. In that incident, over 4,000 affected victims, some contaminated and off-gassing, sought medical treatment without official transport. This means that a very large number of people who either came into contact or had a good chance of coming into contact with sarin were moving freely throughout the city. It is fortunate that the toxicity of the sarin used in the at- tacks was not potent enough to kill many more and the associated off-gassing that occurred resulted in illness and not death.

Citizens seeking medical assistance were not treated by responders prepared with on-scene decontamination assets, causing a high rate of secondary exposure among the medical staff at unspecialized facilities. Containment of the incident area includes, therefore, the ability to bring specialized treatment to the site, because “agent absorbed by cloth may be released as a vapor by the cloth for 30 minutes or more after exposure” (CBWinfo. com). Again, because the sarin was put together quickly

and was only 30% pure, the agent did not lead to any serious injuries to people not in direct contact with the dispersal device. However, it is startling that such an impure chemical mixture was able to affect over 20% of the hospital workers treating victims who hadn’t been in direct contact with the sarin dispersal device and had been transported from the scene over an extended period of time. The lesson is clear—in responding to an attack in which biological, chemical, or radiological weapons are suspected, establishing control of the traffic of people both in and out of the area is crucial for the protection of the scene victims and those would-be victims in the surrounding communities.

Secondary Devices or Threats Perhaps the most pressing and worrying element of con- cern is that of secondary devices and threats targeting responders and evacuating civilians. Terrorism poses a distinct, highly dangerous hazard and challenge in itself, but the potential for secondary attacks and fall- out aimed at even more casualties to responders further complicates the big picture and attempts to control the aftermath. Terrorism aims to cause as much damage or harm to as many people as possible, so a follow-up attack should be a primary consideration, not merely considered a marginal possibility.

The previously mentioned example of Eric Rudolph and his involvement in abortion clinic bombings is rel- evant here as well. The detonation of a bomb outside of an Atlanta night club 1 week after the women’s clinic blast where a secondary attack was successful provided responders with enough warning to suspect a similar tactic in the Atlanta night club bombing. Fortunately, the responders remained diligent, and the secondary device that Rudolph allegedly planted was located and ren- dered safe before it killed or injured responders. Similar terror tactics were used extensively by several interna- tional terrorist organizations, most notably the Real Irish Republican Army and the Colombian paramilitary gue- rilla group known as the Revolutionary Armed Forces of Colombia. Real Irish Republican Army guerilla forces “have operated a two-bomb strategy, hoping secondary devices ‘catch’ security forces rushing to the scene of the first” (CNN). The adoption of such tactics by the enemies of the United States, given their resourcefulness and excellent access to information, should certainly not be discounted.

Regardless of the recent elevated concerns and atten- tion given to this phenomenon, preparation for such a scenario was lacking. In the aftermath of the collapse of the World Trade Center towers, the initial rescue phase was followed by a massive recovery effort. Within a day

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or so after the two towers collapsed, there were already thousands of workers on the scene. Following the at- tacks, estimates placed the number of volunteers and workers from all disciplines at ground zero at 30,000 to 40,000. At the same time, however, “risk of second- ary attack was not made a priority as the rescue effort was vigorously pursued” (Senay). The buildings in the immediate vicinity were not searched for 4 days; it took months to clear all structures properly. There was no standard procedure for obtaining resources such as mili- tary aid to augment this task and expeditiously proceed with the search and clearance process.

Failure to secure a perimeter immediately and control site access, as just mentioned, left avenues open through which to strike. In addition, the ma- jority of the nation’s federal response and leadership to the disaster was housed in two Manhattan hotels surrounded by response vehicles brightly decorated with a wide variety of responding agencies’ logos, decals, and identifying placards. The worst kept se- cret in the city of New York was where all the federal responders were resting, recuperating, and spending their down time. There is no question that a well- planned or even a last-minute secondary attack would have produced a very high number of casualties due to the large number of vulnerable personnel in the area. Such an attack would have crippled the New York response, but more importantly, the secondary attack at that particular time would have crippled the nation due to the message it sent to those not directly affected by the events in New York and Washington, DC, elevating the appearance of capacity and potency of the terrorist attackers.

Numerous tactics could be applied in a secondary attack. The potential for snipers to receive training and apply it with startling effect was demonstrated by the killing spree undertaken by the Beltway snipers, John Allen Muhammad and Lee Boyd Malvo. Powerful and ac- curate weapons such as shoulder-fired rocket-propelled grenades and American-made Stinger missiles, in addi- tion to heavily proliferated small arms, are obtainable through the international black market and have been

proven to be deadly in small-scale guerilla conflicts in Africa, the Middle East, and across the globe. Suicide attacks come in many forms, including vehicle-borne improvised explosive devices and explosives strapped on or secreted in the body of an individual; both tactics have proven to render devastating effects. It is clear, therefore, that there is both a real threat and a worrisome example in which this threat was not prepared for sufficiently. The NYPD report makes this apparent: “NYPD lacked systematic intelligence and threat assessment function and had difficulty assessing risk of further terrorist at- tack in weeks after 9/11” (McKinsey & Company). But given this historical perspective and embracing a desire to enhance response safety, readiness, and capacity, the contemporary emergency response leader can use these events and context as a platform for moving ahead with refinement of existing plans to address gaps that might exist to afford their communities and responders a better degree of safety.

Chapter Summary

Operational security and site security are the most im- portant concepts that are engaged through a conscien- tious, comprehensive effort to protect and secure vital infrastructure before, during, and after a catastrophic event. To ensure that OPSEC and site security is a con- cept that is embraced and promoted, dialogue with all traditional and nontraditional response agencies should occur on an ongoing basis prior to “game day.” These meet-and-greet-and-break-bread gatherings require the checking of egos at the door and the establishment of a real goal-oriented working session. Where possible, agencies should assign, support, and fund the position of OPSEC officer to address and coordinate these respon- sibilities. This requirement also includes the creation of memoranda of understanding detailing the roles, du- ties, and responsibilities of all agencies and responders assisting in the development of long-term working relationships all aimed at security, safety, and preserva- tion of life.

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Wrap Up Chapter Questions

1. List and discuss the definitions of OPSEC and site security.

2. Discuss the differences between OPSEC and site security.

3. List and discuss the five steps of the OPSEC process.

4. Diagram and subsequently discuss the compo- nents of the intelligence cycle.

5. Identify what agency is charged with fostering widespread adoption of OPSEC at the national, state, tribal, territorial, and local agency levels. What support does it provide to these constituent agencies?

6. Discuss why site security is an important strategic and tactical consideration at emergency response scenes.

7. Outline the critical components of establishing and sustaining site security operations and how they integrate into the incident command system process.

8. Discuss the importance of evidence protection and the value emergency responders afford law enforcement when responders take protective measures to recognize and preserve suspected evidence at the scene of an incident.

9. Identify and discuss the importance of personal accountability at the scene of an incident and how OPSEC and site security can augment this process. Additionally, describe what measures

for personnel authentication can be employed by integrating OPSEC and site security into local response policy and operational doctrine.

Chapter Project I

Develop a sample OPSEC policy for your agency that addresses each of the five steps in the OPSEC process. Remember to allow for integration of mutual aid re- sponse assets into the protocol.

Chapter Project II

Review a past large-scale incident, examining the re- sponse for site security compliance. Discuss the pros and cons of the response and how you would improve/ enhance the site security operation.

Vital Vocabulary

Intelligence The product resulting from the collection, collation, evaluation, analysis, integration, and interpre- tation of collected information.

OPSEC A tool designed to promote operational effec- tiveness by denying adversaries publicly available indica- tors of sensitive activities, capabilities, or intentions.

Public information officer (PIO) The position within the incident command system responsible for providing information about the incident. The PIO functions as a point of contact for the media.

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Weapons of Mass Effect— Chemical Terrorism and Warfare Agents Paul M. Maniscalco Dr. Christopher P. Holstege Dr. Frederick R. Sidell

• Understand the importance of preparedness for a chemical attack.

• Recognize the characteristics of nerve agents.

• Outline victim treatment procedures for nerve agent exposure.

• Outline treatment procedures for cyanide exposure.

• Define vesicants and list the symptoms for exposure to specific vesicants.

• Recognize the symptoms of exposure to pulmonary agents.

• Define the common riot control agents.

• Recognize the importance of triage in mass victim incidents.

Objectives

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Introduction

Chemical warfare agents are chemical substances that were developed for use on the battlefield to kill, injure, or incapacitate. For 79 years, from their first use in 1915 in World War I until 1993, the intentional use of these chemicals to kill, injure, or incapacitate was limited to battlefield use. The requisite tactics and necessary tech- nology for chemical terrorism events are unmistakably notable from using chemical weapons designed to meet military needs. Chemical terrorism can be defined as an asymmetric warfare tactic employed by nonmilitary actors against noncombatant (civilian) targets.

At the first World Trade Center attack in New York City in 1993, the attackers integrated cyanide into the construct of the explosive device they manufactured. Fortunately, the expected dissemination did not effi- ciently occur with the violent explosion; the explosion rapidly consumed the integrated product, rendering the tactic ineffective. In June 1994, the religious cult Aum Shinrikyo disseminated one of these agents, sarin, throughout an apartment complex in Matsumoto, Japan, with the intent of causing widespread harm or death to people. In March 1995, the same group released sarin on the Tokyo subways, causing injuries in over 1,000 people and death in 12. Terrorists had a new weapon—a chemical weapon.

Rogue individuals and organizations continue to possess or have access to these weapons. There are prob- ably several dozen countries with the capacity to manu- facture these chemicals, and some of these countries are known to be sponsors of terrorist groups and acts of terrorism. In addition, instructions for the synthesis of these agents are widely available to terrorist groups and rogue individuals in books, on the Internet, and in other places such as militia newsletters.

Some very toxic chemicals are regularly manufac- tured in large amounts in this country and are trans- ported daily on our highways and railways. Chemicals such as cyanide, phosgene, and chlorine, all of which were once military agents, are widely used in large amounts (CP FIGURE 8-1). Many commonly used pesticides have very similar properties to nerve agents.

With the ever-increasing number of toxic chemicals in the world and the existence of rogue organizations that are willing to use them to further their causes, it is

essential that communities and emergency response or- ganizations prepare to confront the challenges presented by a chemical terrorist event.

Terrorist incidents involving military chemical agents are, from an individual victim treatment founda- tion level, not much different from a regular hazardous materials incident; victim care is the same. The criti- cal differences are: (1) it is a deliberate release and (2) most likely it is a high-impact/high-yield incident with numerous victims.

Overall, there are differences between an accidental spill of a toxic chemical and a deliberate release of the same chemical. Probably the most important difference is the fear and anxiety generated in the community and among the emergency responders who must deal with unknown factors. This fear and anxiety may be present in possible victims, who do not know and who can- not be immediately reassured that they have not been harmed, or it might be present in responders who fear a secondary hostile device at the scene designed to in- jure them. Many more agencies become involved in a deliberate release incident, including emergency medi- cal services (EMS), fire/rescue, emergency management, law enforcement, and all levels of government that will converge on the scene in an effort to assist. The site of a deliberate incident is a crime scene, a chemical hot zone, a biological hot zone, and in most cases a high-impact/ high-yield multiple casualty incident. These events result in EMS and the medical community playing a significant lead role in consequence management. Between delayed onset of symptoms, decontamination practices, victim tracking, and other relevant activities, EMS and hospitals must remain attentive to victim signs and symptoms that may indicate a sentinel event of an attack.

Delivery/Dissemination Chemical agents are disseminated in many ways. Bombs, rockets, mines, and other explosive devices are used by the military. When these explode, some of the agent remains as liquid, some immediately evaporates to form vapor, and some will exist as small droplets of the agent suspended in air, or an aerosol. These small droplets eventually evaporate and become a vapor. The result is a hazard from the liquid agent, both as the original liq- uid and as the aerosol droplets (which neither remain long nor travel far) and a hazard from agent vapor. Agents can also be sprayed from airplanes during battlefield use, as some agents were during the Vietnam War.

Liquid chemical agents might be employed with an explosive device by nonmilitary users. The user would have to make the device, which is not without hazard, and then detonate it in the right place at the right time.

The emergency response community must be prepared for a consequence response to a chemical attack.

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Other means of disseminating the agent are more likely. Insecticides are sprayed from airplanes and helicopters in both crop dusting (FIGURE 8-1) and mosquito eradication. This is an obvious and expensive way to disseminate an agent, but it is effective for spreading it over a large area providing the weather and winds are favorable. Vehicle- mounted spray tanks can be driven through the streets of a target area to disseminate an agent. For example, in Matsumoto, the agent was spread from the back of a vehicle in which a container of agent was heated (to help it to evaporate), and the vapor was blown through the street by a fan. Indoor areas might be attacked by putting an agent in the air system, and rooms could be thoroughly and quickly contaminated by the use of a common aerosol spray can. There are other methods of disseminating liquids.

Nerve Agents Nerve agents are toxic materials that produce injury and death within seconds to minutes. The signs and symptoms caused by nerve agent vapor are characteristic of the agents and are not difficult to recognize with a high index of suspicion. Very good antidotes that will save lives and reduce injury if administered in time are available.

Nerve agents are a group of chemicals similar to, but more toxic than, commonly used organophosphate insecticides such as Malathion. Nerve agents were de- veloped in Germany during the 1930s for wartime use, but they were not used in World War II. They were used in the Iran–Iraq war. They were also used by the religious cult Aum Shinrikyo in Japan on two occa- sions; the first use injured about 300 people and killed seven in Matsumoto in June 1994; the second killed

12 and injured over 1,000 in the Tokyo subways in March 1995.

The common nerve agents are tabun (GA), sarin (GB), soman (GD), GF, and VX (GF and VX have no common names) (CP FIGURE 8-2).

The nerve agents are liquids (not nerve gases) that freeze at temperatures below 0°F and boil at tempera- tures above 200°F (CP FIGURE 8-3). Sarin (GB), the most volatile, evaporates at about the rate of water, and VX, the least volatile, is similar to light motor oil in its rate of evaporation. The rates of evaporation of the oth- ers lie in between. In the Tokyo subway attack, sarin leaked out of plastic bags and evaporated. Serious injury was minimized because the rate of evaporation of sarin is not rapid, so the amount of vapor formed was not large. If the sarin had evaporated more rapidly (e.g., like gasoline or ether), much more vapor would have been present, and more serious injury in more people would have occurred.

Nerve agents produce physiological effects by in- terfering with the transmission between a nerve and the organ it innervates or stimulates, with the end result being excess stimulation of the organ. Nerve agents do not actually act on nerves. Instead, they act on the chemical connection of the nerve to the muscle or organ. Normally, an electrical impulse travels down a nerve, but the impulse does not cross the small synaptic gap between the nerve and the organ. At the end of the nerve, the electrical impulse causes the release of a chemical messenger, a neurotransmitter, which travels across the gap to stimulate the organ. The organ may be an exocrine gland, a smooth muscle, a skeletal muscle, or another nerve. The organ responds to the stimulus by secret- ing, by contracting, or by transmitting another message down a nerve. After the neurotransmitter stimulates the organ, it is immediately destroyed by an enzyme so that it cannot stimulate the organ again. Nerve agents inhibit or block the activity of this enzyme so that it cannot de- stroy the neurotransmitter or chemical messenger. As a result, the neurotransmitter accumulates and continues to stimulate the organ. If the organ is a gland, it contin- ues to secrete; if it is a muscle, it continues to contract; or if it is a nerve, it continues to transmit impulses. There is hyperactivity throughout the body.

FIGURE 8-1 Crop dusting is an obvious and expensive way to disseminate an agent, but it is effective for spreading it over a large area providing the weather and winds are favorable.

Remember that it does not take an explosive device to disseminate chemical agents. There are multiple methods of disseminating chemical agents over a wide area.

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Nerve agents perform the following actions within the human body:

• Block the activity of an enzyme (called acetyl- cholinesterase)

• Cause too much neurotransmitter to accumu- late (acetylcholine)

• Cause too much activity in many organs, glands, muscles, skeletal muscles, smooth mus- cles (in internal organs), and other nerves

In the presence of nerve agent poisoning, exocrine glands secrete excessively. These glands include the tear glands (tearing), the nasal glands (rhinorrhea or runny nose), the salivary glands (hypersalivation), and the sweat glands (sweating). In addition, the glands in the airways (bronchorrhea) and in the gastrointestinal tract secrete excessively in the presence of nerve agents.

The clinically important smooth muscles that re- spond are those in the eye (to produce small pupils, or miosis), in the airways (to cause constriction), and in the gastrointestinal tract (to cause vomiting, diarrhea, and abdominal cramping).

Skeletal muscles respond initially with movement of muscle fibers (fasciculations, which look like rip- pling under the skin), then twitching of large muscles, and finally weakness and a flaccid paralysis as the mus- cles tire.

Nerve agents affect the following: • Lacrimal glands (tearing) • Nose (rhinorrhea) • Mouth (salivation) • Sweat glands (diaphoresis) • Bronchial tract (in airways causing wheezing) • Gastrointestinal tract (cramps, vomiting, diar-

rhea) • Skeletal muscles

Fasciculations, twitching, weakness, paraly- – sis

• Smooth muscles Airways (constriction) –

• Central nervous system Loss of consciousness – Convulsions – Cessation of breathing –

Among the nerve-to-nerve effects are stimulation of autonomic ganglia to produce adrenergic effects such as hypertension (high blood pressure) and tachycardia (rapid heart rate). The exact mechanisms in the central nervous system are less well defined, but the result is loss of consciousness, seizures, cessation of breathing (apnea) because of depression of the respiratory center, and finally death. Early effects also include stimulation of the vagus nerve, which causes slowing of the heart

(bradycardia), or stimulation of the sympathetic system to cause tachycardia.

The effects that occur depend on the route of exposure and the amount of exposure. The initial ef- fects from a small amount of vapor are not the same as those from a small droplet on the skin, and the initial effects from a small amount of vapor are not the same as those from a large amount of vapor. Exposure to nerve agent vapor produces effects within seconds of contact. These effects will continue to worsen as long as the victim is in the vapor atmosphere but will not worsen signifi- cantly after the victim is removed from the atmosphere.

Exposure to a small concentration of vapor will cause effects in the sensitive organs of the face that come into direct contact with the vapor—the eyes, the nose, and the mouth and lower airways. Miosis (small pupils) is the most common sign of exposure to nerve agent vapor. Reddened, watery eyes may accompany the small pupils, and the victim may complain of blurred and/or dim vision, a headache, and nausea and vomiting (from reflex mechanisms). Rhinorrhea (runny nose) is also common, and after a severe exposure the secre- tions might be quite copious. Increased salivation may be present. Agent contact with the airways will cause con- striction of the airways and secretions from the glands in the airways. The victim will complain of shortness of breath (dyspnea), which, depending on the amount of agent inhaled, may be mild and tolerable or may be very severe. These effects will begin within seconds after contact with the agent. They will increase in severity while the victim is in the vapor, but will maximize within minutes after the victim leaves the vapor.

Sudden exposure to a large concentration of vapor, or continuing exposure to a small amount, will cause loss of consciousness, seizures, cessation of seizures with cessation of breathing and flaccid paralysis, and death. After exposure to a large concentration, loss of con- sciousness occurs within seconds, and effects progress rapidly to cessation of breathing within 10 minutes.

Vapor Exposure Small Concentration

• Miosis (red eyes, pain, blurring, nausea) • Runny nose • Shortness of breath • Effects start within seconds of contact.

Large Concentration

• Loss of consciousness • Convulsions • Cessation of breathing • Flaccid paralysis • Effects start within seconds of contact.

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A very small, sublethal droplet of agent on the skin causes sweating and muscular fasciculations in the area of the droplet. These may begin as long as 18 hours after agent contact with the skin and generally will not be noticed by either the victim or medical personnel. A slightly larger, but still sublethal droplet will cause those effects and later cause gastrointestinal effects, such as nausea, vomiting, diarrhea, and cramps. The onset of these are also delayed and may start as late as 18 hours after exposure. A lethal-sized droplet causes effects much sooner, usually within 30 minutes of contact. Without any preliminary signs, there will be a sudden loss of consciousness and seizures followed within minutes by cessation of breathing, flaccid paralysis, and death.

Effects from skin contact with a liquid droplet will occur even though the droplet was removed or decon- taminated within minutes after contact. Rapid decon- tamination will decrease the illness but will not prevent it. Nerve agent liquid on skin will cause effects that begin many minutes to many hours after initial contact. After the effects begin they may worsen because of continued absorption of agent through the skin.

Liquid on Skin Very Small Droplet

• Sweating, fasciculations • Can start as late as 18 hours after contact

Small Droplet

• Vomiting, diarrhea • Can start as late as 18 hours after contact

Lethal-Sized Droplet or Larger

• Loss of consciousness • Convulsions • Cessation of breathing • Flaccid paralysis • Usually starts without warning within 30

minutes Management of a nerve agent casualty consists of

removing the agent from the victim (decontamination) or the victim from the agent, administration of anti- dotes, and ventilation if needed. EMS providers must have proper personal protective equipment during these operations.

For the antidotes to be effective, the victim must be removed from the contaminated area and/or the agent must be removed from the victim’s skin. Although the antidotes are quite effective, they cannot overcome the effects of the agent while the victim is continuing to breathe the agent or while the agent is still being ab- sorbed through the skin. Skin decontamination will not remove an agent that has been absorbed into the

skin. Even if the agent is not yet through the skin, effects may start as long as several hours after skin decontamination.

Removing the victim from the area of contamination or the vapor area should be rather simple in a normal hazardous materials incident, but the complexities of a mass casualty terrorism event present some unique challenges. If the agent was released inside a building or other enclosed space, moving the victims outside should suffice. If the agent was released outside, victims should be removed and triaged far upwind.

Removal of the agent from the skin must be done as early as possible. It is unlikely that you will see a liv- ing victim with visible amounts of nerve agent on his skin. However, if this occurs, remove it (the substance) as quickly as possible. Flushing with large amounts of water or wiping it off with dirt or any other convenient substance will help. If clothing is wet, suggesting agent exposure, remove the clothing as quickly as possible. This should be done in the hot zone before the victim reaches the decontamination site in the warm zone. Although the agent is removed from the surface of the skin, the agent that has already penetrated into the skin cannot be removed, and absorption will continue; the victim may worsen despite antidotes.

The antidotes for nerve agent poisoning are atro- pine and an oxime, 2-pyridoxime chloride or 2-PAMCl (Protopam). They act by different mechanisms. Atropine blocks the excess neurotransmitter and protects the site on the organ that the neurotransmitter stimulates. As a result, the glands dry and the smooth muscles stop contracting (such as those in the airways and gastroin- testinal tract). However, atropine has little effect on the skeletal muscles, and these muscles may continue to twitch despite an adequate dose of atropine.

The initial dose of atropine is 2 mg to 6 mg. This dose might seem high to those accustomed to admin- istering it for cardiac or other purposes, but it is the amount necessary to overcome a total-body excess of the neurotransmitter. After the initial dose, a dose of 2 mg should be administered every 5 to 10 minutes until (1) the secretions have diminished considerably, and (2) breathing has improved or airway resistance has decreased (if the victim is being ventilated). Tachycardia (rapid heart rate) is not a contraindication to atropine

Treatment for nerve agent exposure involves decontami- nation, administration of antidotes, and ventilation.

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use in these victims. Atropine can be administered by an intramuscular (IM) route, an intravenous (IV) route, or by an endotracheal route. Atropine administered by IV to animals hypoxic from nerve agent poisoning has caused ventricular fibrillation, so good advice is not to administer it by this route until ventilation has begun.

The oxime, 2-PAMCl, attacks the complex of the agent bound to the enzyme and removes the agent from the enzyme. As a result, the enzyme can resume its normal function of destroying the neurotransmit- ter. Despite the fact that this drug sounds like a very effective antidote, it does not reverse the effects seen clinically in the glands and smooth muscle. It does re- duce the skeletal muscle twitching and weakness. It is almost totally ineffective when used against poisoning from one nerve agent, soman (GD), but it is unlikely that identification of the agent will be made before the initial therapy, and use of the oxime in the usual doses will do no harm.

The initial dose of 2-PAMCl is 1 gram given slowly (over 20 minutes or longer) in an IV drip. More rapid administration will cause hypertension (which can tran- siently be reversed by phentolamine). The 2-PAMCl should not be titrated with the victim’s condition as atropine is, but it should be administered at hourly in- tervals for a total of three doses.

A third drug, diazepam (Valium) or a similar benzo- diazepine anticonvulsant, should be used for any convul- sions and as rapidly as possible.

The military originally had an autoinjector device called the MARK I with two spring-powered injectors, one containing atropine (2 mg) and the other 2-PAMCl (600 mg) (CP FIGURE 8-4). The latest iteration of this countermeasure is a single unit autoinjector with two chambers called the “antidote treatment—nerve agent, autoinjector” (ATNAA). The ATNAA provides atropine injection and pralidoxime chloride injection in separate chambers as sterile, pyrogen-free solutions for intramus- cular injection. The ATNAA is a specially designed unit for automatic self-administration or buddy administra- tion by military personnel. When activated, the ATNAA sequentially administers atropine and pralidoxime chlo- ride through a single needle. There is a civilian version of the ATNAA that is called the DuoDote, manufactured by Meridian Medical Technologies, which is intended as an initial treatment of the symptoms of organophosphorus insecticide or nerve agent poisonings (CP FIGURE 8-5).

The autoinjector is a very effective and fast way to administer the antidotes, and use of this causes the drugs to be absorbed faster. Instructional material for both the ATNAA and DuoDote can be found in the reference section of this text.

When treating an unconscious victim severely af- fected by nerve agent poisoning, gasping for air or not breathing, seizing or postictal, the responder should take care of the airway, breathing, and circulation first. When an airway is inserted and ventilation is attempted in a severe nerve agent victim, the airway resistance will be so great that most devices used for ventilation will not be effective, making ventilation impossible. It might be best to IM administer the antidotes first. This ensures that some air will be moved when ventilation is attempted.

A victim might be exposed to vapor only and be out of the vapor environment and be walking and talking when first seen. This victim might be relatively asymp- tomatic or may be very uncomfortable from shortness of breath but generally is in no danger of loss of life. There may be miosis with red, watery eyes, rhinorrhea, a head- ache or eye pain, nausea and vomiting, and shortness of breath with auscultatory sounds of airway constriction and secretions. Atropine (2 mg, IM or IV) will reduce or eliminate the shortness of breath and most of the rhinor- rhea, but not the eye effects (miosis, pain) or the nausea and vomiting. The responder should start 2-PAMCl (1 gram, slow IV drip).

Initial Antidote Use Vapor Exposure

• Miosis and/or runny nose—no antidotes unless eye pain is severe (eye drops)

• Shortness of breath—2 or 4 mg of atropine de- pending on severity; 2-PAMCl by slow drip

• Unconscious, convulsions, severe breathing difficulty; moderate to severe effects in two or more systems—6 mg of atropine IM; 2-PAMCl by slow drip; ventilation

Liquid on Skin

• Local sweating, fasciculations—2 mg of atro- pine; 2-PAMCl by slow drip

• Vomiting, diarrhea—2 mg of atropine; 2-PAMCl by slow drip

• Unconscious, convulsing, severe breathing difficulty; moderate to severe effects in two or more systems—6 mg of atropine IM; 2-PAMCl by slow drip; ventilation

In all cases, follow with 2 mg of atropine every 5 to 10 minutes until improvement occurs using the amount of wheezing (bronchospasm) as an indicator of when to administer subsequent doses.

Systemic atropine (IM, IV, and endotracheally) has almost no effect on the eyes unless large amounts are administered. If eye pain/headache or nausea and vomit- ing are severe, these are relieved by topical application of atropine or homatropine eye ointment. These medi-

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cations will cause severe blurring of vision for about 24 hours, and it is best not to administer them unless the pain or vomiting is severe. The slight reduction in vision (dimness, slight blurring) caused by the agent is less than that caused by the medications. Miosis by itself (without pain or nausea) should not be treated.

If dyspnea is more than moderate and if the victim is still capable of walking and talking, the initial dose of atropine should be 4 mg. Whether the initial amount is 2 mg or 4 mg, an additional 2 mg should be adminis- tered in 5 to 10 minutes if there is no improvement in the victim’s condition. More should be given at similar intervals if necessary, but in most instances the initial 2 mg will reduce the symptoms.

A more severely affected victim will be unable to walk or talk. He will be unconsciousness with severe breathing difficulties or not breathing, perhaps convuls- ing or postictal with copious secretions and muscular twitching. A severely affected victim may also be one who has moderate or severe signs in two or more organ systems (respiratory, gastrointestinal, muscular, and central nervous systems). The eyes and nose are not considered in this evaluation. This victim should ini- tially be given 6 mg of atropine (IM, not IV), and an IV drip containing 1 gram of the oxime should be started. Ventilation begins after the antidotes are administered. Diazepam or a similar anticonvulsant should be admin- istered. Atropine should be continued at 5- to 10-minute intervals until there is improvement.

A small liquid droplet on the skin will cause sweat- ing and fasciculation at the site, and if this is noted, the victim should receive atropine (2 mg, IM) and 2-PAMCl (1 gram in a slow IV drip). A slightly larger droplet initially will cause gastrointestinal effects (nausea, vomiting, diarrhea, cramps), and a victim with these symptoms should receive the same drugs in the same amounts. A victim with either the small droplet or the larger droplet might worsen, and atropine should be continued at intervals. The onset of these effects may be as long as 18 hours after contact with the agent. Any victim suspected of contacting a liquid agent should be kept under observation for 18 hours.

A large, lethal-sized droplet of agent will cause sud- den loss of consciousness followed by seizures, cessation of breathing, flaccid paralysis, and death. These effects begin within 30 minutes of contact with the agent, and there are usually no preliminary effects before the loss of consciousness. Management is the same as for severe vapor exposure, with early decontamination if therapy is to be successful.

You can save a victim with a heartbeat by timely and adequate therapy. Occasionally an arrested victim

can also be saved. One victim from the Tokyo subway incident had no heartbeat when he was taken into the hospital, but he was adequately treated. He walked out of the hospital several days later.

Cyanide

Cyanide, like the nerve agents, can cause serious illness and death within minutes. Cyanide was not successful as a warfare agent in World War I for several reasons, including: (1) it is volatile and tended to evaporate and be blown away by a breeze; (2) it is lighter than air and will not stay close to the ground where it can do dam- age; and (3) the dose to cause effects is relatively large, and, unlike other agents, it causes few effects at lower doses.

Some forms of cyanide are gases under temperate conditions (hydrogen cyanide, cyanogen chloride), and other forms are solids (sodium, potassium, or calcium cyanide). Hundreds of thousands of tons of cyanide are manufactured, shipped, and used worldwide annually. It is used in the manufacture of certain synthetic prod- ucts, paper, and textiles; in tanning; in ore extraction; in cleaning jewelry; in printing; and in photography. It is in the seeds of some foods and is in the cassava plant—a staple in certain parts of the world. It is produced when synthetic materials (e.g., plastics) burn. Cyanide has been associated with killing. For centuries it has been used for assassinations and is used in the gas chamber for executions. People sometimes ingest cyanide with sui- cidal intent. It was taken by the followers of the Reverend Jim Jones for suicide and was illicitly placed in Tylenol bottles in the Chicago area years ago.

The human body has a means of detoxifying or neutralizing small amounts of cyanide, and this is very effective until the system is overwhelmed. The body combines cyanide with a form of sulfur, and the nontoxic product is excreted. When the body runs out of sulfur, effects appear.

Cyanide causes biological effects by combining with an enzyme that is in cells, and stopping or inhibiting its activity. This enzyme normally metabolizes oxygen in the cell so that the cell can function. When cyanide stops the activity of this enzyme, the cell cannot func- tion and dies. There is plenty of oxygen available in the blood, but the cell cannot use it so it does not take it from the blood.

The effects of exposure to a small concentration of vapor or the initial effects from drinking cyanide are relatively nonspecific. They include a brief period of rapid onset, gasping respiration, tachycardia, anxiety,

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altered mental status, seizures, hypotension, dysrhyth- mias, chest palpations/tightness, tachypnea, diaphoresis, low pulse oximetry even with presence of oxygen, skin pale to slightly reddish color, deep breathing, feelings of anxiety or apprehension, agitation, dizziness, a feeling of weakness, nausea with or without vomiting, and muscu- lar trembling. As more cyanide is absorbed, conscious- ness is lost, respiration decreases in rate and frequency, and seizures, cessation of breathing, and disturbances in heart rate and rhythm follow. After inhalation of a high concentration of vapor, seizures can occur within 30 seconds, and cessation of breathing and disturbances of cardiac rhythm follow. Death occurs in 6 to 10 minutes after exposure.

Large Amount by Inhalation

Hyperventilation: 15 seconds Convulsions: 30 seconds Cessation of breathing: 3–5 minutes Cessation of heartbeat: 6–10 minutes

Management

Hydroxocobalamin 5g IV or Amyl nitrite pearl Sodium nitrite IV (10 mL; 300 mg) Sodium thiosulfate IV (50 mL; 12.5 g) and Ventilation with oxygen Correction of acidosis

Cyanogen chloride causes the effects of cyanide as listed previously. However, it is very irritating (similar to the riot control agents) and will produce burning of the eyes, the nose, and airways. It has a pungent odor.

There are few findings on physical examination. The skin is said to be cherry red (because of the red, oxygen- ated venous blood), but this is not always present. The pupils are normal in size or slightly large, secretions are relatively normal, and there are no muscular fascicula- tions, all of which serve to distinguish cyanide poisoning from nerve agent poisoning.

In the laboratory, cyanide can be measured in blood. Also, there will be more than the normal amount of oxygen in venous blood, and there may be a metabolic acidosis. Management consists of removing the victim from the contaminated atmosphere (or by removing the poison from the victim), and administering antidotes and oxygen.

Hydroxocobalamin

Hydroxocobalamin, a vitamin B12 precursor, is now available in multiple countries as an antidote for cyanide poisoning. In 2006, it was approved by the U.S. Food

and Drug Administration. Hydroxocobalamin com- plexes cyanide, forming cyanocobalamin (vitamin B12). One molecule of hydroxocobalamin binds one molecule of cyanide. The U.S.-approved adult starting dose is 5 g administered by IV infusion over 15 minutes. Depending upon the severity of the poisoning and the clinical re- sponse, a second dose of 5 g may be administered by IV infusion for a total dose of 10 g. Hydroxocobalamin has few adverse effects, which include allergic reaction and a transient reddish discoloration of the skin, mucous membranes, and urine. No hemodynamic adverse ef- fects other than a potential mild transient rise of blood pressure are observed.

The Cyanide Antidote Kit

The cyanide antidote kit (CP FIGURE 8-6) contains the fol- lowing three components: (1) amyl nitrite; (2) sodium nitrite; and (3) sodium thiosulfate. Amyl nitrite is avail- able in a pearl. This should be broken and placed in a breathing bag for the victim to inhale. Instructions state that this should be held under the victim’s nose for him or her to breathe. Sodium nitrite is packaged in an ampule containing 300 mg in 10 mL for IV administra- tion. Amyl nitrite should be used only until the sodium nitrite can be administered by IV. The third component is a sulfur compound, sodium thiosulfate. When this is administered, the body can resume the normal pro- cess of tying up cyanide with sulfur to form a nontoxic substance. An ampule contains 12.5 g in 50 mL for IV administration. These three antidotes should be given sequentially to a victim who is unconscious and/or not breathing. Oxygen should be administered, even though the oxygen content of blood is normal. The acidosis should be corrected.

Vesicants

Vesicants are agents that cause vesicles or blisters. They may be of animal, vegetable, or mineral origin, such as some types of sea creatures, poison ivy, and certain chemicals. Other things, such as sunlight, can produce blisters. Vesicants have been used as chemical warfare agents. Several have been developed for this purpose, but only one—sulfur mustard (CP FIGURE 8-7)—has been used. The other major chemical warfare vesicant is lewisite.

Cyanide antidotes are: hydroxocobalamin or amyl ni- trites, sodium nitrite, and thiosulfate.

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Sulfur mustard was first synthesized in the early 1800s and was first used on the battlefield in World War I. During that war it caused more chemical casualties than any other agent; however, only about 3 percent of these casualties died. Iraq used it extensively during its war with Iran, and pictures of some casualties were in the media during that period. Its use has been alleged in some other conflicts over the past 80 years.

In the early 1940s, nitrogen mustard (developed for military use), a close relative of sulfur mustard, was used in the treatment of cancer, the first chemical to be used for that purpose.

Sulfur mustard (mustard) is a light yellowish to brown oily liquid that smells like garlic, onions, or mus- tard (the reason for its name). Its boiling point is over 200°F, and it freezes at 58°F. The low freezing point hinders its battlefield use in cool weather, and it is often mixed with another chemical to lower the freezing point. It does not evaporate very quickly, but large amounts of mustard, particularly in warm weather, produce a vapor hazard.

Mustard causes cellular damage and death with sub- sequent tissue damage. The mechanism by which it does this has not been entirely clear, but the best evidence suggests that it damages DNA, which then prevents further cellular functioning and leads to cellular death. Although its best-known effects are those on the tissues, the agent directly contacts the skin, the eyes, and the airways. When it is absorbed into the body in adequate amounts, mustard damages many tissues such as bone marrow, lymphoid tissue, and the gastrointestinal tract. Its effects are similar to those caused by radiation, and it is a radiomimetic agent.

Once liquid or vapor mustard is in contact with an epithelial surface, the skin, the eye, or the mucosa of the airways, it penetrates that surface quite rapidly, and enough is absorbed within a minute to cause cel- lular damage. Decontamination after a minute will not prevent tissue damage, but it will reduce the amount of ensuing damage. Once into tissue, the chemical reactions within the cell that eventually result in clinical effects begin. Once mustard touches a body surface, irreversible damage is done in cells within minutes.

Upon contact with the skin, the eyes, or the airways, mustard causes no immediate clinical effects. There is no immediate pain, redness, or blister formation. The victim

usually does not know he or she has been exposed. The itching and pain of erythema, the irritation of the con- junctiva, or the irritation and discomfort in the upper airways do not appear until many hours later. The period without signs or symptoms is called the latent period, and it can range from 2 to 24 hours after contact. Com- monly these effects begin in 4 to 8 hours after contact.

At the site of an incident or spill involving mus- tard, there will be no victims with signs and symptoms of mustard exposure. Hours later, the pain, irritation, and discomfort will start, and the victims will seek medical care.

The initial effects in the eyes after exposure to mus- tard vapor are irritation or burning, and the victim will complain of grittiness in his eyes. The eyes will be red, similar to the appearance of eyes with sand or dust in them. This may progress to a severe conjunctivitis, swelling of the lids, and even corneal edema (seen as an irregular light pattern on the cornea). The victim will complain of pain, irritation, and sensitivity to light. He may also complain of inability to see. This is usu- ally because the lids are shut, either because of swelling or because of involuntary contracture of the muscles around the eye. Rarely, a droplet of mustard will get into the eyes, and this may cause more severe damage to the cornea, including ulceration and perforation.

Mustard contact with skin will initially cause redness, or erythema, which is similar to sunburn with burning and itching. If the contact was to a low concentration of vapor, this may be the extent of the injury, but more commonly small blisters develop around the edges of the redness. These gradually coalesce to form larger blisters, which are generally no worse than second degree burns. Third degree burns are very uncommon and require exposure to a large amount of liquid agent.

Mustard vapor, when inhaled, damages the mucosa or inner layer of the airways. The damage begins at the upper part of the airways (the nose) and descends to the lowermost portion, the terminal bronchioles. The amount of damage depends on the amount of mustard inhaled, which, in turn, depends on the concentration of the vapor and exposure time. The initial effects are in the nose and sinuses with burning, irritation, and perhaps some nasal bleeding. Pharyngitis, with a sore throat and a nonproductive cough, may appear, followed by laryngitis with hoarseness or complete lack of voice. Mustard damage in the lower airways causes shortness of breath and a cough productive of inflammatory and necrotic material as the agent de- stroys the inner lining of these small airways. Severe damage provides an ideal setting for infection 4 or 5 days later.

Vesicants cause vesicles or blisters.

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Initial Effects There are no immediate effects of contact with sulfur mustard; effects start potentially hours after contact.

Skin

• Redness (erythema) with burning and itching • Blisters

Eye

• Redness with burning and itching

Airways

• Nasal and sinus pain • Sore throat, nonproductive cough Large amounts of absorbed mustard severely damage

the precursor cells in the bone marrow, with a decrease in the white cells, red cells, and platelets in the blood. This usually happens four or more days after exposure in a severely exposed victim. The lining of the gastroin- testinal tract is also severely damaged after absorption of a large amount of mustard with subsequent loss of fluid and electrolytes starting days after exposure. This effect is similar to that seen after radiation exposure.

Immediate decontamination—within a minute— should be performed to minimize the damage, but re- sponders will not be on the scene that quickly. Skin damage will be reduced by decontamination of the con- tact site on the skin if done within 30 minutes, but not beyond that time.

A victim returning hours after the incident with red skin (erythema) needs no immediate care, although soothing lotions (e.g., calamine) can be applied to re- duce the burning and itching. Later, areas of blistering or denuded skin must be irrigated frequently, with the application of topical antibiotics three or four times a day to these areas. Fluids do not need to be replaced in large amounts as they do after thermal burns, because mustard burns do not cause the amount of fluid loss seen in thermal burns. Care must be taken not to overhydrate victims. They will not need significant fluid replacement unless they are dehydrated from other causes.

A victim with red eyes (conjunctivitis) who is com- plaining of burning or irritation in the eyes should have his or her eyes washed out and a soothing ophthalmic ointment or drops applied. Because the lesion appears hours after contact with the agent, the agent is no longer in the eye because of absorption and evaporation, and the purpose of eye irrigation is to wash out inflammatory

debris. Later eye care consists of regular application of a topical antibiotic and a mydriatic (to prevent future ad- hesions between lens and iris). Petroleum jelly should be applied regularly to the edges of the lids (to prevent ad- hesions). Some believe that topical steroids used within the first 24 hours only will reduce inflammation, but application should be done by an ophthalmologist.

A suggestion of airway involvement by the agent, such as nasal or sinus irritation or a sore throat with a dry hacking cough, may occur. Laryngeal damage with voice changes or hoarseness accompanied by signs of beginning lower airway damage is an indication for the immediate insertion of an endotracheal tube. Later, more severe damage will necessitate assisted ventilation in- cluding positive end-expiratory pressure and frequent sputum examinations for infecting organisms.

Bone marrow depression and severe gastrointestinal damage occur days after the initial exposure in an already severely ill victim.

All victims must be decontaminated before they enter a medical facility. When signs and symptoms appear hours after the initial agent contact, the agent will be gone from exposed surfaces by evaporation or by absorption. Later decontamination will not prevent further injury to the victim. However, liquid may be in clothing or the agent (liquid or condensed vapor) may be in hair.

Lewisite

Lewisite was developed late in World War I but was not used in that war. Japan possibly used it against China in the late 1930s; otherwise it has not been used on the battlefield. Some countries are known to have military stockpiles of lewisite.

Lewisite is an oily liquid with the odor of gerani- ums. Its freezing point is below 0°F, it boils at 190°F, it contains arsenic, a heavy metal, and it is more volatile than mustard.

Lewisite participates in many biological reactions, but the mechanism of cellular injury is unknown. It damages cells causing cellular death, and its biological effects are similar to those of mustard with topical dam- age to eyes, skin, and airways (CP FIGURE 8-8). It does not damage marrow, the gastrointestinal tract, or lymphoid tissue, but it does damage systemic capillaries allowing leakage of intravascular volume. This can culminate in hypovolemic shock in severe cases.

An important initial clinical distinction between lewisite and mustard is that lewisite vapor causes imme- diate irritation of eyes, skin, and upper airways. Lewisite

Immediate decontamination is very important with mustard exposure.

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liquid causes pain or burning on whatever surface it con- tacts within seconds. The victim is alerted to its presence and will leave the area or remove the liquid. Mustard causes no clinical effects until the lesions develop, hours after contact.

Lewisite causes topical damage to eyes (conjunc- tivitis and more severe damage), skin (erythema and blisters), and airways (damage to the lining or mucosa) similar to that of mustard. Severe lewisite exposure may cause pulmonary edema, which is very uncommon after mustard exposure. Generally, the lesions from lewisite are deeper with more tissue damage than those from mustard.

Management of a victim with lewisite exposure is similar to the management of a victim with mustard exposure. The victim will usually self-decontaminate quickly because of the pain or irritation. In addition to the measures recommended for mustard lesions, there is a specific antidote for the systematic (nontopical) ef- fects of lewisite. This is British antilewisite, a drug used for several other types of heavy metal poisoning, and is for hospital use only.

Pulmonary Agents

Pulmonary agents are chemicals that produce pul- monary edema (fluid in the lung), with little damage to the airways or other tissues. The best known and most studied of these is phosgene (carbonyl chloride), although other chemicals (e.g., chlorine) behave in this manner.

Phosgene and chlorine were major agents in World War I until the use of mustard. Their usefulness as war- fare agents has diminished since then, and now they are not considered important militarily. However, both are important in industry, and large amounts of both are manufactured and shipped annually.

After inhalation of phosgene, the carbonyl part of the molecule causes damage in the thin wall between the blood vessels (capillaries) and the air sac (alveolus). As a result of this damage, the watery part of the blood leaks into the alveoli. When these become filled with fluid, air cannot enter to deliver oxygen to the blood, oxygen cannot be delivered to other tissues, and the victim suf- focates in a sense. This fluid in the lungs is similar to

that seen in drowning. Damage by these agents is some- times called “dry-land drowning.” Another name for this is noncardiac pulmonary edema, which is pulmonary edema (fluid in the lung tissue) caused by something other than heart failure.

A high concentration of phosgene causes an immedi- ate irritation in the eyes, nose, and upper airways. This is usually transient and is followed later by pulmonary edema. An extremely high concentration will cause la- ryngeal edema and death within a short period of time, but this is very uncommon. The usual circumstance is that the victim inhales phosgene without immediate ef- fects. Anywhere from 2 to 24 hours later, the victim begins to become short of breath. Initially, he or she notices the shortness of breath only with walking or other exertion, but as time passes, it is present at rest. A cough brings up clear, frothy sputum—the fluid that leaked into the lungs. If the symptoms begin late, after 6 or 8 hours, the damage is usually not severe enough to cause death, but if the effects begin early, from an hour to 6 hours after exposure, the lung damage is often severe enough to cause death despite medical care.

Initial Effects Initial effects of pulmonary agents include the following:

• Shortness of breath with exertion, later at rest • Cough, later with production of frothy sputum A responder at the site may see few symptomatic

victims, except possibly some with irritation of the eyes and upper airways or some exposed to extremely high concentrations who will soon have laryngeal edema. Most casualties will be minimally symptomatic, and the tendency might be to discharge them from care. This could well be a mistake. Symptoms can start suddenly, and if they begin within the first several hours, death may occur within the next several hours. Anyone who has been exposed to one of these agents must be kept under medical observation for at least 6 hours.

A victim exposed to a pulmonary agent will have two major problems for hospital management. The first is the fluid in the lungs (pulmonary edema) with resulting lack of oxygen (hypoxemia). The second is loss of fluid from the intravascular space (hypovolemia), which may lead to hypotension, shock, and organ damage.

Initial management of victims is twofold. The first and hardest thing to remember is that anyone possibly exposed to one of these agents should be kept at abso- lute rest with absolutely no exertion. The victim must be carried, not walked, to the ambulance. It is hard to tell a healthy person at the site of a spill or incident who has no symptoms that he or she cannot walk, but it must be done. World War I experience with these casualties

Lewisite causes eye and upper airway irritation and pain on contact.

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shows that a victim breathing comfortably in bed might collapse and die if allowed to walk down the hall to the bathroom.

The second and more obvious part of managing a pulmonary agent victim is to provide oxygen to anyone who is short of breath. This usually will not happen while the responder is on the scene initially, but may happen when the responder provides transport later.

Riot Control Agents

Most people are familiar with riot control agents, otherwise known as tear gas or irritants. Three are in common use in this country. CS (or 2-chlorobenzal- malononitrile—also called o-chlorobenzylidene ma- lononitrile) is used by law enforcement agencies and the military; phenacyl chloride—also called Mace—was used in World War I and is now in small spray devices carried for self-protection; and pepper spray, which is replacing the others for both law enforcement and mili- tary use and for self-protection.

Unlike other agents that are liquids, these are solids. The powdery particles are suspended in liquids when they are in spray devices. These agents have much in common. Their effects begin within seconds of contact, the effects last only a few minutes after the person is in fresh air, they are effective in small concentrations, and the lethal concentration is thousands of times higher than the effective concentration, which means that ac- cidentally producing an overdose is very unlikely.

These agents cause irritation, pain, or burning on surfaces they contact, including the eyes, the nose, the mouth and airways, and the skin. Eye effects include burning, tearing, redness, and an initial involuntary temporary closing of the eyes (blepharospasm). While the eyes are closed, the victim cannot see and might be considered incapacitated. The interior of the nose burns, and there are secretions from the nose. There are secre- tions from the mouth, and the interior of the mouth burns. If the agent is inhaled, there will be coughing and perhaps a feeling of shortness of breath. There is an initial burning or tingling on the skin accompanied by a mild redness. Sometimes a high concentration will cause retching or gagging. The effects will gradually recede in 15 to 30 minutes after exposure has ceased.

There are potential complications that seem to be rare. If the face is close to the agent when it is dispersed with force (e.g., a spray device), the force may drive the particles into the eye. This necessitates flushing with copious amounts of water or manual removal of the particle by an ophthalmologist. The agent might pre- cipitate a severe reaction in a person with chronic lung disease (chronic obstructive pulmonary disease, asthma, etc.) including hyperactive airways. The use of oxygen, assisted ventilation, and bronchodilators might be in- dicated. A person exposed to a high concentration in a hot and humid environment might develop a delayed dermatitis beginning about 6 hours after contact, with erythema developing into blisters.

People can develop tolerance to these agents. With continued exposure, the effects lessen and the exposed people can open their eyes and function relatively normally.

Triage

Triage is an ongoing process that begins with the first person to see the victim and continues through hospi- tal management. The responder will triage at several places, including in the hot zone, in the cold zone after the victim has been decontaminated, and possibly in between. In the hot zone, the responder is encumbered with protective clothing and victim examination is not ideal. The following triage categories are generally used: immediate, delayed, and minimal.

An immediate victim is one who is in danger of loss of life unless there is intervention within a short period of time. Intervention generally has to do with airway, breathing, and circulation (the ABCs), and to this the administration of antidotes should be added. A delayed victim is one who can wait for intervention, and this wait will not affect the outcome of care. The victim is stable but will require further care. A minimal victim is one who requires care for a relatively minor injury. The care can be done quickly, the injury is not life threat- ening, and the victim is unlikely to require long-term care (i.e., hospitalization). An expectant victim is one who cannot be saved with the resources available or resources cannot be made available within the time the victim needs them.

Treatment for exposure to pulmonary agents is oxygen and immediate rest (no exertion).

Effective triage of chemically exposed victims is crucial in mass victim events.

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Nerve Agents An immediate victim is one who (1) is unconscious, is apneic or struggling to breathe, is convulsing or has convulsed, and has muscular twitching or is flaccid; or (2) has moderate or severe signs in two or more organ systems (respiratory, gastrointestinal, muscular, and central nervous system). This victim should be given 6 mg of atropine—IM, not IV—and a 20- to 30-minute drip of 1 g of 2-PAMCl.

A delayed victim is one who is recovering from mod- erate or severe effects or from the effects of several doses of antidote.

A minimal victim is one who is walking and talking. That person may be severely short of breath or vomiting, but still has muscle strength and control and can under- stand the spoken word enough to respond. Generally, this victim should be given 2 mg of atropine with a drip of 2-PAMCl. If the victim is extremely short of breath, 4 mg of atropine should be administered. Despite the shortness of breath, this victim is not immediate.

An expectant victim is one who is not breathing and is without a heartbeat. However, if he or she has been without cardiac activity for a very brief period of time, every attempt should be made to resuscitate the victim.

Cyanide Cyanide victims can die within minutes after inhaling a large concentration of the agent. Those who are uncon- scious and not breathing but who still have a heartbeat should be classified as immediate, and the antidotes should be given as soon as possible. If a victim is con- scious, he or she will be minimal and will not need anti- dotes. An expectant victim is one who has been without a heartbeat for many minutes.

Vesicants Almost all vesicant victims will be delayed. They will need no immediate care, but they will need further care for their eye, skin, or airway injuries. An exception is a victim with moderate to severe airway effects including shortness of breath. He or she is immediate and needs intensive pulmonary care.

Pulmonary Agents Although shortness of breath, the major symptom from these agents, can be faked, anyone complaining of short- ness of breath within 6 hours of exposure should be classified as immediate for intensive pulmonary care. A victim with shortness of breath beginning later than 6 hours postexposure will also need care and monitoring. A victim with severe shortness of breath and copious frothy sputum within an hour after exposure is expect-

ant, although an attempt should be made to provide maximum care.

Riot Control Agents Victims of riot control agents will be usually classified as minimal with the exception of a victim who has a se- vere airway reaction to these agents or a polypharmacy scenario where underlying conditions are exacerbated and possibly require immediate care.

Early Recognition When first responders in protective gear first enter the hot zone, they usually will not know what the toxic agent is and usually will not have a detector to tell them. They must quickly evaluate the victims based on what is seen and heard and take appropriate action. Early therapeutic intervention is needed for only two types of agents—nerve agents and cyanide. A victim exposed to a large concentra- tion of a pulmonary agent may be in severe respiratory distress, but there is nothing that can be done in the hot zone; if the effects started before the responder arrived, probably nothing can be done elsewhere.

In most chemical mass casualty situations, the vic- tims will exhibit a spectrum of effects. Some victims’ conditions will be quite severe, and others will have minor effects, and the responder must quickly evaluate this spectrum. For example, if some victims are convuls- ing or are unconscious and appear to be postictal, the responder should look at other victims. The presence of miosis, runny noses, and shortness of breath or any one or two of these strongly suggests that nerve agents were the offending substance. If the conscious victims are relatively normal with a few nonspecific complaints, cyanide should be considered. If all victims are conscious with no complaints, the responder should consider that (1) no chemical agent was present, or it was present in concentrations too low to produce effects, or (2) the agent was one that produces delayed effects only, such as mustard or the pulmonary agents.

If many victims are complaining of irritation or burning in the eyes and nose, on the mucous membranes of the mouth, and on the skin, one might consider the following:

1. Riot control agents (in which case the victims will improve with fresh air)

2. Phosgene (the effects will improve, but there will be later, more severe ones)

3. Cyanogen chloride (the irritation will gradually decrease, and if the victim is conscious when help arrives it is unlikely that a lethal concentration was present)

4. Lewisite (the effects will worsen)

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Refer to TABLE 8-1 for a summary of signs, symptoms, and decontamination procedures for chemical agents.

Chapter Summary

Chemical agents are not new, and terrorist organizations have access to these substances as demonstrated by the use of sarin in a Tokyo subway attack in 1995. Many industrial chemicals such as chlorine, cyanide, phosgene, and pesticides are readily available in large quantities.

It is essential that response agencies be prepared for a chemical attack. Effective planning must include protective equipment, decontamination procedures, and antidotes. A deliberate incident is a crime scene, usually with mass numbers of victims.

Nerve agents are toxic materials that produce injury or death in seconds to minutes. Nerve agents are similar to insecticides but are more toxic.

Very good antidotes are available for nerve agents, but they must be administered quickly. Common nerve agents include tabun (GA), sarin (GB), soman (GD), and GF and VX. Effects from nerve agents show very quickly. Management of nerve agent exposure consists of decon- tamination, administration of antidotes, and ventilation.

The antidotes for nerve agent poisoning are atropine and an oxime, PAMCl (Protopam). Atropine blocks the excess neurotransmitters. PAMC1 removes the nerve agent from enzymes, allowing the enzymes to block the neurotransmitters. Benzodiazepines (i.e., diazepam) can be used as anticonvulsants.

Cyanide can cause serious illness and death within minutes. Cyanide affects the ability of the cells to me- tabolize oxygen. Treatment of cyanide poisoning can in- clude hydroxocobalamin or using the cynanide antidote kit (amyl nitrite pearl or sodium nitrite IV and sodium thiosulfate IV). Victims should be ventilated with oxygen and acidosis should be corrected.

Vesicants are agents that cause vesicles or blisters. The most common vesicant agents are sulfur mustard and lewisite. Mustard does not cause an immediate ef- fect; the common latent period is 4 to 8 hours after contact. Inhaled vapor causes damage to the airway and

bronchioles. Victims must be decontaminated immedi- ately and the eyes irrigated.

Lewisite produces instant effect on contact. The symptoms include immediate pain, eye damage, and airway injury.

Pulmonary agents produce pulmonary edema. The best-known agents are phosgene and chlorine. The ef- fects of these agents are not immediate, but shortness of breath followed by pulmonary edema follows hours after exposure. Exposed victims with no symptoms must be kept under medical observation for at least 6 hours. Initial victim treatment includes keeping the victim at rest and administering oxygen.

Riot control agents are known as tear gas and ir- ritants. They include tear gas, Mace, and pepper spray. Effects begin in seconds but last only a few minutes after the victim is removed to fresh air. These agents cause pain, burning, and irritation to the contact body surfaces. The use of oxygen is indicated.

Triage is an ongoing process in a chemical exposure incident. The triage categories are immediate (critical), delayed, and minimal (walking wounded). A critical victim is one who is unconscious, apneic, or convuls- ing. Almost all vesicant victims will be delayed. Most riot control victims will be in the minimal or walking wounded category.

Early responders must quickly evaluate the scene. Rapid therapeutic intervention is needed only for nerve agents and cyanide. If a victim shows severe pulmonary distress from a pulmonary agent, nothing can be done in the prehospital setting.

The use of positive pressure ventilation and albuterol nebulizers has been shown to improve the noncardiac pulmonary edema condition. The extent of treatment offered by a responder is dependent upon the type of incident, number of victims and your local treatment and MCI protocols. The learner is encouraged to review the guidance documents provided by local authorities.

In mass casualty incidents, victims will exhibit a spectrum of effects. Responders must quickly don pro- tective equipment and triage all victims to determine treatment categories.

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TABLE 8-1 Chemical Agents: Symptoms and Treatment

Agent Signs and symptoms Decontamination Immediate treatment/ management

Nerve agents (GA, GB, GD, GF, VX)

Vapor: Small exposure— Miosis, rhinorrhea, and mild dyspnea. Large exposures— Sudden loss of consciousness, convulsions, apnea, flaccid paralysis, copious secretions, and miosis. Liquid on skin: Small to moderate exposure— Localized sweating, nausea, vomiting, and feeling of weak- ness. Large exposure—Sudden loss of consciousness, convul- sions, apnea, flaccid paralysis, and copious secretions.

Large amounts of water with a hypochlorite solution.

Administration of atropine and pralidoxime chloride (2-PAMC1); diazepam in addition if casualty is severe; ventilation and suction of airway for respiratory distress.

Mustard (HD, H) Asymptomatic latent period (hours). Erythema and blisters on the skin, irritation, conjunctivitis, corneal opacity, and damage in the eyes; mild upper respiratory signs, marked airway damage; also gastrointestinal effects and bone marrow stem cell suppression.

Large amounts of water with a hypochlorite solution.

Decontamination immediately after exposure is the only way to prevent/limit injury/ damage. Symptomatic management of lesions.

Lewisite (L) Lewisite causes immedi- ate pain or irritation of skin and mucous membranes. Erythema and blisters on the skin and eyes and airway damage similar to those seen after mustard exposure develop later.

Large amounts of water with a hypochlorite solution.

Immediate decontami- nation; symptomatic management of lesions the same as for mustard lesions; a specific antidote British antilewisite (BAL) will decrease systemic effects.

Phosgene oxime (CX) Immediate burning and irritation followed by wheal-like skin lesions and eye and airway damage.

Large amounts of water. Immediate decontami- nation; symptomatic management of lesions.

Cyanide (AC, CK) Initially may have dyspnea, weakness, and dizziness.

Skin decontamination is usually not neces- sary because agents are highly volatile. Wet, contaminated cloth- ing should be removed and the underlying skin decontaminated with water or other standard decontaminates.

Antidote: intravenous sodium nitrite and sodium thiosulfate. Supportive care: oxygen and correct acidosis.

Pulmonary agents (CG)

Eye and airway irritation, dyspnea, chest tightness, and delayed pulmonary edema.

Vapor: fresh air. Liquid: copious water irrigation.

Termination of exposure, ABCs of resuscitation, enforced rest and observation, oxygen with or without positive airway pressure for signs of respiratory distress, other supportive therapy as needed.

(continues)

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120 Homeland Security: Principles and Practice of Terrorism Response

TABLE 8-1 Chemical Agents: Symptoms and Treatment (continued)

Agent Signs and symptoms Decontamination Immediate treatment/ management

Riot control agents (CS, CN)

Burning and pain on exposed mucous membranes and skin, eye pain and tearing, burning nostrils, respiratory discomfort, and tingling of the exposed skin.

Eyes: thoroughly flush with water, saline, or similar substance. Skin: flush with copious amounts of water, alkaline soap and water, or a mildly alkaline solution (sodium bicarbonate or sodium carbonate). Generally, decontamination is not required if wind is brisk.

Usually none is necessary; effects are self-limiting.

Source: Medical management of chemical casualties handbook, 2nd ed. (1995). Aberdeen Proving Ground, MD: Chemical Casualty Care Office, United States Army Medical Research Institute of Chemical Defense.

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Wrap Up Chapter Questions

1. Discuss several reasons why your community should be prepared for a terrorist chemical attack.

2. What are the methods of disseminating a chemi- cal agent?

3. Define nerve agents. How do they act on the body?

4. List five common nerve agents. 5. What are the symptoms of nerve agent expo-

sure? 6. What is the treatment for nerve agent exposure?

Name three antidotes. 7. Discuss the symptoms of cyanide poisoning.

What are the antidotes for cyanide exposure? 8. What are vesicants? What are the signs of vesicant

exposure? What is the treatment? 9. Define lewisite. How does lewisite exposure differ

from mustard exposure? 10. What are pulmonary agents? What is the treat-

ment for severe exposure? 11. List three riot control agents. What are the symp-

toms and treatment for exposure? 12. What are the triage categories in a chemical attack

with mass victims? Describe typical symptoms of a victim in each category.

Chapter Project

You are an EMS training officer in an organization that has no chemical attack training program. Your goal is to develop guidelines for first response fire units and EMS units. Develop a written chemical response guideline that includes the following key elements:

• Categories of chemical agents • Symptoms at onset and long-term symptoms • Advanced life support care for each type of

agent including antidotes • Basic life support treatment procedures • Safety guidelines • Triage categories and related symptoms

Vital Vocabulary

Cyanide A toxic material, like the nerve agents, can cause serious illness and death within minutes, but is also volatile and lighter than air.

Hydroxocobalamin A vitamin B12 precursor that is now available in multiple countries as an antidote for cyanide poisoning.

Lewisite An oily liquid with the odor of geraniums that contains arsenic and a heavy metal and is more volatile than sulfur mustard.

Nerve agents Toxic materials that produce injury and death within seconds to minutes.

Pulmonary agents Chemicals that produce pulmonary edema (fluid in the lung), with little damage to the air- ways or other tissues.

Riot control agents Solids suspended in liquids as powdery particles; often used in spray devices and used commonly in the United States.

Sulfur mustard (mustard) A light yellowish to brown oily liquid that smells like garlic, onions, or mustard and causes cellular damage and death with subsequent tissue damage.

Vesicants Agents that cause vesicles or blisters.

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Weapons of Mass Effect— Biological Terrorism Dr. Charles Stewart Paul M. Maniscalco Hank T. Christen

• Define the concept of biological warfare.

• Know the history of biological warfare.

• Understand and be able to apply the concepts of biological threat assessment.

• Define the importance of biological protective equipment.

• Outline the types of biological agents including the chemical effects, detection, and prophylaxis/treat- ment of botulinum toxins, Clostridium toxins, ricin, saxitoxin, staphylococcal enterotoxin, tetrodotoxin, and trochothecene mycotoxins.

Objectives

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124 Homeland Security: Principles and Practice of Terrorism Response

Introduction

The uses of biological substances as weapons pose a unique problem for the emergency response and pub- lic health communities. Unlike the consequences of a chemical attack or an explosion, which are essentially readily identifiable, in-your-face events, biological ter- rorism creates a slow-motion riot that builds with each hour after the event. The inability to quickly and im- mediately identify what has occurred allows the threat maturation process to continue while increasing the risk to a vulnerable population.

Biological terrorism is the use of etiological agents (disease) to cause harm or kill a population, food, and/or livestock. Biological terrorism includes the use of organ- isms such as bacteria, viruses, and the use of products of organisms—toxins.

Biological terrorism has recently become more threatening to the world. One only needs to consider the current state of technology, the future possibilities of biotechnologies, and what appears to be a readiness on the part of some individuals/countries to utilize this technology as a weapon.

Successful genetic engineering has arrived, and ad- vances are being achieved almost daily. It requires a relatively easy process and only crude technology to manufacture a lethal organism/toxin in sufficient quan- tities. Some are specifically designed to be resistant to antibiotics for use as a horrible weapon. It has been said that “if you can make beer, you can make bugs (biological weapons).” This is an oversimplification, but it provides a vivid picture of what a motivated person with modern technology is capable of achieving. A recent phenomenon has emerged with the availability of equip- ment and the reduced costs associated with acquiring the same; it is referred to as “garage science.” A simple Internet search easily reveals the extent of experimen- tation and activities that are associated with aspiring biology hobbyists. You can find individuals hacking DNA while others are conducting a variety of organic experiments—all interesting—but highly illustrious of the fact that technology can be exploited to help and hurt if the players are nefarious. Do-it-yourself biotechnology is now happening and encouraged by forums like DIY Bio, Biopunk, and others.

Biological weapons (BWs) have the potential to wreak considerable havoc and death among humans, resulting in a medical disaster. Moreover, should BWs be employed against livestock or vegetation, the results would be an economic disaster.

BWs are more deadly and financially efficient, pound for pound and dollar for dollar, than chemical

agents or even nuclear weapons. It has been estimated that 10 grams of anthrax could kill as many people as a metric ton of the nerve agent sarin. BWs are relatively inexpensive and easy to manufacture, and dispersal devices can be disguised as agricultural or pest-control sprayers. A human carrying the disease is also a disper- sal agent. Unfortunately for the law-abiding world, it is very difficult, if not impossible, for an intelligence service to detect research, production, or transporta- tion of these agents for rogue intentions. It is equally hard to defend against these agents once they have been employed due to the inability to readily recognize delivery.

History of Biological Agents as Weapons The use of biological agents as a warfare weapon has a long and deadly past. In fact, history has shown us that use of BWs occurred more than 2,000 years ago. Some examples of its employment include:

1. In the 6th century B.C., Assyrians poisoned enemy wells with rye ergot (U.S. Army, 1996); Solon used the purgative hellebore during the siege of Krissa (U.S. Army).

2. Persian, Greek, and Roman authors quote the use of animal cadavers to contaminate water supplies. In 1155, Barbarossa used the bodies of dead soldiers to poison the wells at the battle of Tortona.

3. The Scythian archers would dip their arrows in blood mixed with manure or in decomposing cadavers.

4. The Mongols in the 1300s catapulted plague vic- tim corpses into the city of Kaffa to infect the defenders (U.S. Army). The besieged town was rapidly devastated by disease.

5. British and early American settlers gave American Indians blankets used by victims of smallpox. The resultant infection decimated the defenseless American Indian tribes.

6. In 1941, the Allies tested anthrax on Gruinard Island off the shore of Scotland (Bernstein, 1987). Starting in 1986, a determined effort was made to decontaminate the island, with 280 tons of formaldehyde solution diluted in seawater being sprayed over all 520 acres (2 km²) of the island, and the worst-contaminated topsoil around the dispersal site being removed. A flock of sheep was then placed on the island and remained healthy. On April 24, 1990, after 48 years of quarantine, junior defense minister Michael Neubert visited the island and announced its safety by removing the warning signs (Harrison, 2001).

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7. During World War II, the Allies administered 235,000 doses of antitoxin to Allied troops and deliberately leaked this information to the Nazis. Simultaneously, they told the Nazis that the Allies were prepared to use BWs if they were employed in the war (Mobley, 1995).

8. During World War II, on the Pacific front, the Japanese tested BWs on prisoners of war in China, killing more than 1,000 people. In fact, it has been reported that the Japanese had “stockpiled 400 kilograms of anthrax to be used in specially designed fragmentation bombs” (U.S. Army, 1996).

9. Unclassified information from Central Intelligence Agency and Defense Intelligence Agency docu- ments indicates that several rogue states such as Iran, Libya, and North Korea have or are pursuing BW programs (Horrock, 1997).

10. In September and October of 1984, followers of the Bhagwan Sri Rajneesh contaminated restau- rant salad bars in Oregon. More than 750 people were intentionally infected with Salmonella.

11. In 1994, a Japanese sect of the Aum Shinrikyo cult attempted an aerosolized release of anthrax from the tops of buildings in Tokyo.

12. In 1995, two members of a Minnesota militia group were convicted of possession of ricin, which they had produced themselves for use in retaliation against local government officials.

13. In 1996, an Ohio man attempted to obtain bu- bonic plague cultures through the mail.

14. In 2001, anthrax was delivered by mail to U.S. media and government offices (FIGURE 9-1A, 9-1B, and 9-1C). There were five deaths. The first victim, Robert Stevens, worked at American Media Inc., in Boca Raton, Florida. Two were distribution clerks in the Brentwood postal facility in Washington, DC. Joseph P. Curseen, 47, died at the Southern Maryland Hospital Center in Clinton, Maryland, and Thomas L. Morris Jr., 55, died at the Greater Southeast Community Hospital in Washington, DC. Kathy Nguyen, 61, died October 31, 2001. She was a New York hospital worker who con- tracted inhalation anthrax. The last victim, Ottilie Lundgren, 94, died November 21, 2001, at Griffin Hospital in Derby, Connecticut.

In recent times, the military examined the possibil- ity of biological actions against the United States. In the 1950s, Serratia and Bacillus species were released from ships in the San Francisco Bay area and caused at least one death (Cole, 1988). In the 1960s, military researchers introduced B. subtilis into New York City

subway ventilator shafts. Both passengers and security guards were oblivious to the danger (Cole, 1985). The bacteria were rapidly spread to the ends of the subway system, successfully demonstrating the ability to exploit that environment with these substances.

The U.S. Office of Technology Assessment has estimated that a small private plane with 220 pounds of anthrax spores, flying over Washington, DC, on a

FIGURE 9-1A Anthrax letter sent to Tom Brokaw.

FIGURE 9-1B Anthrax letter sent to Senator Tom Daschle.

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126 Homeland Security: Principles and Practice of Terrorism Response

windless night, could kill between 1 and 3 million peo- ple and render the city uninhabitable for years.

Other countries are certainly continuing to develop biowarfare capabilities. The Soviets and their allies em- ployed a trichothecene mycotoxin dubbed “yellow rain” in Laos, Cambodia, and Afghanistan, and the former USSR and Iraq have independently developed anthrax species. In 1979, an outbreak of inhalational anthrax oc- curred in Sverdlovsk, Russia. This outbreak resulted from an accident at a Soviet biowarfare research facility.

Treaties

The Geneva Convention (1925) prohibited the use of biological and chemical warfare. In 1972, the United Nations Convention on the Prohibition of the Development, Production and Stockpiling of Bacteriological (Biological) and Toxin Weapons and on Their Destruction (a.k.a. the Biological and Toxin Weapons Convention) was executed with an imple- mentation date of March 26, 1975. By June 2005, there were 171 signatories, and 155 of these had ratified the convention to stop development, production, and stockpiling of chemical and bacteriological (biologi- cal) weapons. Research for defensive purposes is still allowed and continues across the globe.

Treaties and multilateral agreements cannot com- pletely rid the world of chemical weapons and BWs,

which are simple, inexpensive, and produced by widely available technology. Nor will they fully eradicate the threat of individuals who fervently desire to acquire and use them as weapons. Here are some recent ex- amples:

Paris police, in 1984, raided a suspected safe house for the German Red Army Faction. During the search they found documentation and a bathtub filled with flasks containing Clostridium botulinum (Douglas, 1987).

Russia’s biological warfare technology may be vul- nerable to leakage to third parties through either theft or outright sale (like nuclear materials), as a result of the fi- nancial crises that exist. Open-source intelligence reports that army personnel and scientists have been known to sell off military equipment to get money to feed their families. In some cases, reports have been received that these individuals, in critical and sensitive positions, have not been paid in months, making them vulnerable to recruitment by rogue organizations or nations.

The Aum Shinrikyo cult members (famous for the sarin gas attack in Tokyo subways) were found to have anthrax and botulinum cultures when the Japanese national police conducted their raid of the Aum base camp at the foot of Mount Fuji. They had constructed dedicated laboratories and had purchased a helicopter equipped with a spraying apparatus. The Aum had also visited Zaire during the Ebola outbreak to collect speci- mens of Ebola virus (Flanagin & Lederberg, 1996).

In the town of The Dalles, Oregon, in 1984, more than 750 people became sick after eating in four differ- ent restaurants. The illness was traced to the Bhagwan Sri Rajneesh sect, which had spread salmonella on salad bars in the four restaurants (Cole, 1996). The intention of this group was to sicken many of the community to prevent them from going to the polls, thus interfer- ing with the political process and manipulating a local election.

A U.S. microbiologist named Larry Wayne Harris fraudulently ordered three vials of bubonic plague cul- tures by mail in 1995 (Horrock, 1997). The ease with which he obtained these cultures prompted new legis- lation to ensure that biological materials are destined only for legitimate medical and scientific purposes. These products are often shipped via commercial delivery com- panies such as UPS and FedEx, which is perfectly legal.

In December 2002, six terrorist suspects were ar- rested in Manchester, England; their apartment was serv- ing as a ricin laboratory. Among them was a 27-year-old chemist who was producing the toxin.

On October 15, 2003, a ricin-laced letter, addressed to the Department of Transportation in Washington,

FIGURE 9-1C Anthrax letter sent to the New York Post.

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DC, U.S.A., was intercepted at a mail sorting facility in Greenville, South Carolina. The letter, which threatened future ricin attacks if the government didn’t pass pend- ing trucking legislation, was signed by Fallen Angel.

On February 3, 2004, three U.S. Senate office build- ings were closed after the toxin ricin was found in the mailroom that serves Senate Majority Leader Bill Frist’s office.

Threat Assessment

Although the conclusion that the United States is very vulnerable to a biowarfare attack or terrorism is indis- putable, the BW programs of the 1950s and 1960s were appropriately criticized for the unethical exposure of unwitting test subjects. Despite the escalating BW threats and the experiences of the anthrax attacks of 2001, our level of preparedness is still insufficient given the po- tential harm and disruption that could be realized in the aftermath. With limited capacity to anticipate a biologi- cal attack, little or no ability to detect one if it occurs (unless the perpetrators decide to announce the release and take credit for their demonic acts), and a dimin- ished ability to effectively manage the consequences if attacked, this problem poses a series of complex issues that need immediate review. There are a number of rea- sons for this unpreparedness, which will be discussed in the following sections.

Intelligence When a BW manufacturing facility can be constructed in the area of a large garage, law enforcement/intelli- gence services are confronted with great difficulty in locating it. Accessing cultures is not nearly as expen- sive or tracked as well as nuclear material. BW culture processing requires equipment that would be consid- ered suitable for a well-equipped hospital laboratory or academic research facility and is thus easily ordered and diverted. If this does not sound credible, please take some time to research the many events of missing samples from labs, black market activities, and incidents where individuals have exploited loopholes in the system to acquire samples under fraudulent terms (Harris & Paxman, 1982).

As the threat of terrorism has evolved over the years, so has the role of EMS in support of interagency opera- tions. The importance of seamlessly integrating EMS representation into intelligence functions such as state, regional, and local intelligence fusion centers is a critical requirement to ensure the vertical and horizontal flow

of essential information. For instance, tying in to the 911 dispatch data system to monitor call volume and activity with the ability to drill down on data from past years to quickly conduct a correlative analysis of activi- ties for aberrancy is an important data node. Given that most EMS systems operate and staff on the margins, the sensitivity of call volume and the fragility of the system provide a source for rather quick alerts that something is not right. Drawing those EMS data along with emer- gency department activity data into a central location for the EMS representative to coordinate and collaborate on the end operations analysis with the public health representative could be that single, important clue that provides a community early notification of an incident. In the end, that early alert could mean the difference between quick response and control or expansion into a citywide/regional problem or worse.

Detection Detection of biological agents occurs most often after a release. Quite simply, presently there are limited tech- nologies that can detect the deployment of a bacterial agent in the civilian community under normal operat- ing procedures. The only truly accurate means of de- tection is through the clinical presentation of patients, and that will be retrospective for most of the casual- ties. Some limited battlefield detection devices exist, but these are unusable in the majority of U.S. cities. These devices can be effective for special events such as the Olympics, a presidential inauguration, or where crowds are moderately constrained, but due to cost and availability, they have limited benefit to local emergency response organizations. When threat assessments are quite high and advance notice of the threat exists, use of these items through the National Guard civil support teams or through the Department of Defense is highly recommended.

Biological warfare agents are almost undetectable during transit. Likewise, there is no mechanism us- ing routine customs, immigration, drug scan, or bomb search procedures to identify the agent. The only way to find it would be a physical search by a very well- trained and very lucky searcher (Mayer, 1995). Indeed, the agent could be simply sent using FedEx or a similar overnight carrier from one point to another. Even in an event where a package is broken and the product is leaked, law enforcement may have a high index of sus- picion, but identification of the agent will usually take place at a laboratory, not in the field.

A bioterrorism threat might not be directly concen- trated on actual humans. Livestock, crops, and water

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supply are strategic targets and vulnerable to attack. As an example, it is not inconceivable that a rogue indi- vidual or group could attempt to destroy all pork and pork products in the United States. Although this would not be a fatal blow for the United States on the whole, it would certainly not help the U.S. economy to have a porcine plague. Detection of this plague would be very difficult indeed prior to symptoms in a substantial num- ber of the affected animals. (While they should for a number of strategic reasons, few communities include veterinarians in their biological surveillance plans.)

Control of Supplies A military commander maintains the luxury of knowing that his troops are under threat of attack. The civilian emergency response chief does not usually have this warning and the targets for introduction of a biologi- cal agent are almost unlimited. To a large extent, the battlefield commander controls the food and water supply of his troops. To institute such control in the civilian sector would mean martial law, and this is un- acceptable in a free society. This level of freedom is not without cost and it creates vulnerability for rogue groups to exploit.

Personal Protective Equipment Biological terrorism is most likely to be executed co- vertly, and sick individuals may be the initial detector that an attack has occurred. If a biological agent is de- livered effectively, a large number of casualties can be generated in a relatively short period of time depending on the etiologic agent utilized. In the midst of treating the casualties, the emergency responder and organization must not only provide effective care, but also protect themselves and their members.

This will be difficult most of the time due to the unknowing responders believing that they are operat- ing at another sick job. After the release of a bioagent, there is an incubation period in the new host prior to its clinical manifestation. In some cases, this period may be more than 72 hours, and from some agents, it is 2 weeks or more.

One of the limiting factors of personal protective equipment (PPE) is that military issued gear is not certified by the Occupational Safety and Health Administration (OSHA). OSHA certification is a standard requirement for civilian use of any PPE. It has been only recently that some of this equipment is being considered for civil- ian use or “technology transfer,” hence some testing for OSHA standard compliance is taking place (see Chapter 13, “Personal Protective Equipment”).

Regardless, much of the civilian PPE that is available for bioagents is designed for use in the static environ- ment of the laboratory and not the street. This, too, is another issue that will require a cooperative public/ private working arrangement. Clearly, with the threat to the civilian responder escalating, continuing research for better and more functional PPE should be expected with the expertise of military, Homeland Security science and technology, academia, and private industry pooling talent and resources to create a successful resolution of this operational conundrum.

Even if the military or the Centers for Disease Control and Prevention (CDC) provide gear, it must be prepositioned and issued after either a significant threat or after the first casualties have been identified. In either case, there is a significant risk that many of the emergency services (including emergency physicians, nurses, paramedics, and EMTs) will be exposed and become unknowing casualties prior to the arrival of pro- tective gear. Worst-case scenario is that these responders become additional disease vectors, further complicating the overarching response strategies.

Prophylaxis The U.S. General Accounting Office found that at the beginning of the Gulf War in 1991, the U.S. Army’s stockpiles of vaccine for anthrax and botulism had fallen far short of what was needed to protect U.S. troops. Indeed, the General Accounting Office felt that at least 20 percent and perhaps 40 percent of the military’s biowar budget was not directed at dis- eases or toxins that were identified as threats by the military’s own intelligence agencies (Horgan, 1994). Recently, heated discussions have again taken place at the Pentagon and in the media about the need to provide vaccinations to all uniformed service members as a provision of force protection in the face of these BW threats.

Protecting the armed forces against a biological at- tack is less challenging and complex than protecting the civilian population. Military personnel are a captive audience who have little choice regarding whether they will receive an immunization.

At present, we do not have sufficient emergency providers with enough immunizations to provide care for the population of a U.S. city (if attacked) without additional harm coming to the rescuers. These pro- viders will be at the highest risk if an active agent is employed. On the positive side of this discussion, with recent advances in vaccinology, depending upon the threat being confronted, promising countermea-

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sures are starting to be identified as is the ability to administer countermeasures after the exposure has occurred.

Training Emergency responders might be called upon to know treatments for exotic diseases that they are unlikely to have ever encountered. Emergency service members must be aware of symptoms and epidemiological pat- terns that may indicate a biological attack, but many have never been taught these techniques of pattern identification. This creates a heavy reliance upon the expertise of the EMS medical director, the public health director, and the EMS training chief for guidance on next steps and real-time training.

EMS, the fire service, police, and even hospitals must purchase PPE and train employees for work in protective gear that has been found only in the mili- tary and specialized hazardous materials teams. Emergency service organizations must realize that they are significant targets for primary/secondary attacks and should conduct their routine operations appropri- ately while ensuring that the proper security measures are implemented.

Interagency Coordination and Public Perception It is always difficult to balance the perceived needs of multiple population groups. Drawing the fine line between antiwar protesters who feel any research into biowar techniques should be forbidden and those who look for a threat around any corner is always diffi- cult. When given the choice of where to spend defense money, it is easier to put it into real and visible tools such as guns, planes, and troops, playing the CNN factor to the max. In the past, cruise missiles shown on CNN are easier to sell to a congressional committee than protective garments for use in Bloomfield, New Jersey. Even in this post-September 11, 2001 world, we see reluctance on the part of some in Congress about really making the necessary sustainable invest- ments in EMS, medical, public health, and other re- sponder readiness. Hopefully, the momentum that has been attained regarding community bioterrorism and pandemic preparedness will continue to grow, and this view will change so a sustainable capacity can be achieved.

Likewise, control of a program that will spend mil- lions of dollars brings a smile to many bureaucrats’ faces. Will infighting between bureaucratic agencies dissipate any real effort to protect the United States? These issues

require policy decisions with requisite directives to be issued in an effort to set the tone, from the top, ensuring that the process does not become mired in rivalry and competition. Perhaps we can start with a reexamination of the National Response Framework and refine this doc- trine to incorporate an emergency support function that specifically addresses EMS and critical care medicine, while concurrently creating an agency that will have the responsibility for the same and be held accountable for seeing that readiness for this vital function is sustainably accomplished.

When a bioterrorism incident occurs, who will be in charge? Will it be local EMS, fire, police, or emergency management personnel? Will it be medical authorities from state, county, or local departments of health? Will it be medical authorities from the Department of Health and Human Services, CDC, or even military specialists from one of the biowar development centers at Dugway Proving Ground in Utah or Fort Detrick in Maryland? Will the Federal Bureau of Investigation attempt to as- sume control of the scene to preserve evidence? Will the Federal Emergency Management Agency attempt to usurp control of the incident? Will martial law be declared with the military in control of a city? With the recent H1N1 pandemic (2009) it was the secretary of the Department of Homeland Security who was front and center in the management of the federal response coordination. Even with the issuance of Presidential Decision Directive 39, these questions have not been fully and adequately answered.

Command and control issues are always best an- swered in advance of the incident, rather than during the emergency. Having a comprehensive emergency action annex to the existing community emergency manage- ment plan for bioterrorism incidents is strongly encour- aged. Determination of issues such as these should be accomplished before “game day,” not on the field of play. The latter will contribute to the chaos one can expect at this type of incident.

Deniability The existence of naturally occurring or endemic agri- cultural pests or diseases and outbreaks will permit an adversary to anonymously use bioterrorism with com- pletely plausible deniability. Such biological warfare attacks could be against the food supply or crops. The effects of such biological and economic warfare could bring devastation to the affected nation. The Russian wheat aphid has caused over $1 billion in losses in the western United States since it was first discovered/ identified in Texas in 1986. What would a focused and

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deliberate release of a BW agent mean to the economics of the United States?

Response Time Even if an astute emergency physician notes that an unusual number of patients brought in by EMS or as emergency department walk-ins have certain symptoms and contacts the CDC for help, and the crisis is imme- diately recognized as a bioterrorism event, and help is dispatched immediately, the lag time may be unwieldy. With some of the agents that have been identified, there is an incubation period that exceeds 3 days from time of agent distribution until the first cases occur and some agents carry as much as a 20-day period. A patient may be contagious during much of this incubation period with emergency personnel and hospital staff unaware of the jeopardy they are in. Some of the agents have mor- tality rates that approach 100 percent when symptoms go unrecognized.

Given an absolute best-case scenario from notifica- tion, it will take at least 2 hours for a qualified team of predesignated physicians and prehospital providers (paramedics and EMTs) to assemble (this best-case sce- nario occurs only if a community has had the foresight to convene a team prior to the event), ready gear, and respond to the deployment assembly point. It will take another few hours to assess the situation, draw appro- priate clinical samples, and formulate an idea of what illness or toxin was employed. During this time, others will be exposed and potential carriers may be leaving the city, bound for other destinations.

When casualties exceed the available medical re- sources, additional resources must be identified and summoned, and either the patients must be transported to them or the providers and equipment transported to the patients. This scenario will warrant the deployment of federal assets in the form of National Disaster Medical System disaster medical action teams and military units such as the deployable medical teams, if available. All of this will take many hours or days.

If news services broadcast any warning, one can expect a panic-stricken response that may cause gridlock on the roads and further complicate any response team’s travel to the area (and cause a spike in the standard 911 call volume). Essentially, we are looking at a regional, if not national or international emerging health crisis. This statement is very real. Consider the fact that in a conventional weapon attack such as the 1993 World Trade Center bombing, patients were tracked as far west as Pennsylvania and as far north as New Haven, Connecticut.

Response Strategies In addition to the requisite response doctrine for pro- tecting responders are support networks for responders’ families and operational response and logistic sustain- ment tactics that the contemporary emergency response chief or executive must employ in response to a biologi- cal event. Given that the prevailing mantra for response to an infectious event is “social distancing and adminis- tration of countermeasures,” we need to briefly examine the reality of this intervention.

The contemporary disaster response/planning doc- trine involves bringing lots of people and resources to a location where an event has transpired and working our way out of it as quickly as possible. In the event of a bioterrorism incident or a pandemic, the reality of this strategy effectively being employed is ques- tionable due to a number of issues, including but not limited to the scope of the event, limited resources, numbers of people affected, and the large geographic area that could be involved. Currently, conventional wisdom dictates that a social distancing response that is often bantered about translates into a concept we are all familiar with—shelter in place. It is important to note here that sheltering in place is a temporary, limited-duration tactic designed to protect individuals from an immediate pending event such as a gas leak, extreme inclement weather, or other hostile environ- ment. Generally, these events can last a few hours to a day. As discussed previously, given that conven- tional responses and structures are neither designed nor configured to support hundreds if not thousands of individuals staying at home and servicing all of the affected people in disparate locations, the opera- tionalization of the social distancing strategy becomes a complex problem that must be addressed sooner rather than later. Basically, we conduct emergency response operations daily in a “price club” manner, while the social distancing strategy will require us to refine and realign our response patterns and capacity to be more like Meals on Wheels—a retail approach rather than the standard wholesale scheme we utilize to conduct routine operations and run-of-the-mill di- saster response.

It is important that the empowerment of the citizenry to become prepared for a disaster is achieved. Failure to take the necessary steps to create this environment could result in spontaneous and unnecessary evacua- tions of communities and failed or ineffective emergency response capacity.

Although highways leading from an attacked met- ropolitan area are most certainly attractive for citizens

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who feel they need to take matters into their own hands, they will likely be roads to nowhere, leaving citizens trapped and vulnerable. In most cases, remaining in homes or other safe havens in the community will pro- vide the greatest personal security. This is true in terms of physical and emotional safety, because people make their best decisions when they are in stable, familiar environments, and make their worst decisions when in unstable, unfamiliar environments. A strategic concept and operational framework to address the emerging is- sues revolving around extended social distancing re- quirements has been developed out of the University of Virginia’s Critical Incident Analysis Group. The pre- senting model is best described as “shelter in place on steroids” and looks at the series of complex and at times daunting requirements posed by needing to implement a coherent and supported social distancing strategy that will protect and support citizens.

Community shielding is a unique opportunity to engage individuals, communities, and government in a unified response to future acts of terrorism, in particu- lar bioterrorism. The concept envisions an integrated, facilitated form of sheltering, wherein individuals and groups within a community employ a self-imposed iso- lation, or quarantine, within their natural and famil- iar surroundings, for a temporary period of time until a threat or danger abates. The success of community shielding depends upon the development of partner- ships among government, business, the media, and the public, creating an integrated social infrastructure that facilitates a shelter-in-place response by providing es- sential resources to augment individual preparation for natural or unnatural catastrophic events.

Community shielding allows individuals to remain in their homes and communities, rather than evacuat- ing an affected area in an attempt to avoid a threat or danger. Both a government-ordered, mandatory evacu- ation and a spontaneous evacuation of citizens in the absence of instructions to leave an area usually result in a chaotic response, mass movement of citizens on congested roadways to nowhere, and the entrapment of vulnerable citizens suffering from illness or in need of medical care. Gridlock of transportation systems in an affected area also hampers local first responders from reaching those most in need. By contrast, com- munity shielding fosters empowerment and resilience in American citizens to remain at home in their com- munities and fight, rather than to flee, delivering a strong response to defeat the terrorist objective of dis- rupting and destroying American lives and the normal functioning of our society.

Just as individual cells in the body are nourished within organs, so too must places of refuge be sup- ported through community shielding, a wider form of sheltering. When communities are deployed to provide necessary strategic support for sheltering in place, there is less chance for first responders to be overwhelmed by unnecessary and dangerous evacu- ation attempts.

A variety of survey outcome data sources demon- strates a significant increase in the willingness of citi- zens to participate in a community shielding strategy if their sheltering in place is augmented by the provi- sion of resources until it is safe to leave their homes or communities (i.e., delivery of food, water, medica- tions, and medical treatment; dissemination of reli- able information as to the crisis, its duration, and the safety and well-being of family members; and a means to communicate within and outside the affected com- munity). These findings strongly suggest that if local communities’ emergency preparedness and response plans include bringing food, water, medications, and other necessities directly to citizens’ homes and work- places and providing assurances as to the safety and well-being of family members from whom they are separated, citizen response would be favorable and in support of community shielding.

Implementation of community shielding as part of emergency preparedness planning/response to future events will require continued efforts toward a national initiative to increase awareness of the concept and to gain support from key government and commu- nity leaders, as well as the American public. Public education will be necessary to enlist the citizens as significant participants in preparing for such future events, including the dissemination of information as to what steps to take to prepare, how notification of events will be provided, and how communication will be maintained during a crisis. Moreover, the funda- mentals of how to respond to these challenges should be analyzed by the contemporary emergency response chief or executive now in order to allow for realign- ment of planning, training, and operational paradigms to effectively respond to a community in need with shielding implemented.

Realities and Costs It is unlikely that a rational foreign government would risk potential military reprisals and the political/eco- nomic sanctions that overt use of biological warfare against the United States would bring (Lebeda, 1997). Covert action or deniable independent rogue factions

57854_CH09_final.indd 13157854_CH09_final.indd 131 1/20/10 10:29:42 AM1/20/10 10:29:42 AM

F O S T E R , C E D R I C 1 6 9 2 T S

132 Homeland Security: Principles and Practice of Terrorism Response

and transnational terrorist organizations do not have the same constraints. Terrorist organizations operating in a civilian environment have freedom of movement and the ability to use commercially available equipment for development and discharge of their weapon. They are not constrained by a need for precise targeting or pre- dictable results. A determined transnational organization or rogue individual may not be deterred, may escape detection and intelligence-gathering activities, and may succeed in releasing a biological agent in a susceptible target area. Lastly, transnational terrorist groups gener- ally are not affiliated with one country or organization, and as such they have no return address, making a mili- tary retaliation very complicated if not impossible.

The effects of a bioterrorism incident are cata- strophic. In a paper by researchers at the CDC, the projected economic impact alone ranges from $477 million per 100,000 people exposed to brucellosis to $26.2 billion in the case of anthrax (Kaufmann, Meltzer, & Schmid, 1997). Over 30,000 deaths were predicted if anthrax was used as the biological agent. The paper consistently used the lowest possible expense for all fac- tors that affected costs, including the virulence of the disease. Costs of both preparedness and intervention were significant. It is clear that this would not be the case in a real disaster of this magnitude. Even so, the researchers concluded that reducing preventable losses has a significantly greater impact than reducing the prob- ability of an attack through intelligence gathering and prevention strategies.

The authors also noted that the best possible mea- sures to decrease both costs and deaths were those that would enhance rapid response to an attack. “These mea- sures would include developing and maintaining EMS response operation and hospital critical care capacities, laboratory capabilities for both clinical diagnostic test- ing and environmental sampling, developing and main- taining drug medical counter-measure stockpiles, and developing and practicing response plans at the local level” (Kaufmann et al., 1997).

Possible Biotoxins

Until recently, toxins were of interest only to the toxi- cologist, the rare patient who ingested or was exposed to these toxins, and the even rarer writer who discussed toxicological environmental emergencies. Unfortunately, several simultaneous political and scientific events have moved these toxins to a more prominent medical and social position.

Discovery that some of these toxins have been used as agents in warfare or have been stockpiled to use in warfare has given the medical community an impetus to learn more about the effects and production of toxins for biological warfare. New uses for old toxins include botulinum therapy for spastic muscles and dystonia. For an overview of biological symptoms and treatments, refer to TABLE 9-1.

Botulinum Toxins Botulinum neurotoxin is among the most potent toxins known. The mouse lethal dose is less than 0.1 nano- gram per 100 grams. It is over 275 times more toxic than cyanide.

Mueller (1735–1793) and Kerner (1786–1862) in Germany first described botulism. They associated the disease with ingestion of insufficiently cooked blood sausages and described death by muscle paralysis and suffocation. In the early 1900s, botulism occurred com- monly in the United States and nearly destroyed the canned-food industry (Meyer, 1956).

The major source of botulinum toxin is the organism Clostridium botulinum. There are seven serotypes pro- duced by clostridia species. These serotypes are similar but do not cross-react to immune reactions. They are released as a single polypeptide chain of about 150,000 daltons, which is cleaved to generate two disulfide-linked fragments. The heavy fragment (histone 100,000 daltons) is involved in cell binding and penetration, while the light chain is responsible for the toxic intracellular effects.

Clinical Effects

Two natural types of poisoning occur. In the first type, food tainted with clostridia species is stored or processed in a way that allows the anaerobic organisms to grow and multiply. As they grow, they produce and release toxin. If the food is not subsequently heated to destroy the toxin, clinically significant amounts can be consumed. The toxin passes through the gut into the general cir- culation and is distributed throughout the body. In the second type, usually found in infants, the organisms colonize and produce their toxin in the gut. The clinical effects of the two types of botulism are the same.

After ingestion with botulinum toxin, the victim will develop diplopia and ptosis (difficulty speaking and swal- lowing), decreased bowel function, and muscle weakness that can progress to a flaccid paralysis. The patient will generally be awake, oriented, and afebrile. Development of respiratory failure may be quite rapid after initial symp- toms develop. The hallmark sign is progressive, bilateral descending paralysis, which occurs usually within 24 hours of ingesting a contaminated product.

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F O S T E R , C E D R I C 1 6 9 2 T S

CHAPTER 9: Weapons of Mass Effect—Biological Terrorism 133

TA B

LE 9

-1

B io

lo gi

ca l A

ge nt

s: S

ym pt

om s

an d

Tr ea

tm en

t S

ig n

s a

n d s

y m

p to

m s

D ia

g n

o s is

T re

a tm

e n

t P

ro p h

y la

x is

D e c o n

ta m

in a ti

o n

A n

th ra

x In

cu b

a ti

o n

p e

ri o

d is

1 –6

a y

s. F

e v

e r,

m a

la is

e ,

fa ti

g u

e , c

o u

g h

, a n

d m

il d

e st

d is

co m

fo rt

a re

ll o

w e

d b

y s

e v

e re

sp ir

a to

ry d

is tr

e ss

w it

d y

sp n

e a

, d ia

p h

o re

si s,

ri d

o r,

a n

d c

y a

n o

si s.

h o

ck a

n d

d e

a th

o cc

u r

w it

h in

3 6

h o

u rs

o f

se v

e re

m p

to m

P h

y si

ca l f

in d

in g

s a

n o

n sp

e ci

fi c.

P o

ss ib

w id

e n

e d

m e

d ia

st in

u m

. D

e te

ct a

b le

G ra

m s

ta in

o f

th e

b lo

o d

a n

d b

y b

lo o

cu lt

u re

in t

h e

c o

u rs

e o

f il ln

e ss

A lt

h o

u g

h u

su a

ll y

n o

t e

ff e

ct iv

e a

ft e

r sy

m p

to m

s a

re p

re se

n t,

h ig

h -d

o se

n ti

b io

ti c

tr e

a tm

e n

t w

it h

e n

ic il li n

, c ip

ro fl

o x a

ci n

, o

r d

o x y

cy cl

in e

s h

o u

ld b

u n

d e

rt a

k e

n . S

u p

p o

rt iv

th e

ra p

y m

a y

b e

e ce

ss a

ry .

A li

ce n

se d

v a

cc in

e f

o r

u se

t h

o se

c o

n si

d e

re d

a t

ri sk

f o

r e

x p

o su

re . V

a cc

in e

h e

d u

le is

0 , 2

, a n

d 4

e e

k s

fo r

in it

ia l s

e ri

e s,

ll o

w e

d b

y b

o o

st s

a t

6 ,

12 , a

n d

1 8

m o

n th

s, a

n d

e n

a y

e a

rl y

b o

o st

e r.

S e

cr e

ti o

n a

n d

le si

o n

re ca

u ti

o n

s sh

o u

b e

p ra

ct ic

e d

. A ft

e r

a n

v a

si v

e p

ro ce

d u

re o

r a

u to

p sy

is p

e rf

o rm

e d

, th

e in

st ru

m e

n ts

a n

d a

re a

se d

s h

o u

ld b

e t

h o

ro u

g h

d e

co n

ta m

in a

te d

w it

h a

o ri

ci d

a l a

g e

n t

su ch

a s

io d

in e

o r

ch lo

ri n

e .

B o

tu li n

u m

t o

x in

s P

to si

s, g

e n

e ra

li ze

w e

a k n

e ss

, d iz

zi n

e ss

, d ry

o u

th a

n d

t h

ro a

t, b

lu rr

e d

is io

n a

n d

d ip

lo p

ia ,

d y

sa rt

h ri

a , d

y sp

h o

n ia

, a n

d y

sp h

a g

ia f

o ll o

w e

d b

sy m

m e

tr ic

a l d

e sc

e n

d in

fl a

cc id

p a

ra ly

si s

a n

d d

e v

e lo

p m

e n

t o

f re

sp ir

a to

ry f

a il u

re .

S y

m p

to m

s b

e g

in a

s e

a rl

a s

2 4

h o

u rs

, b u

t m

a y

k e

s e

v e

ra l d

a y

s a

ft e

r in

h a

la ti

o n

o f

a t

o x in

C li n

ic a

l d ia

g n

o si

s; n

ro u

ti n

e la

b o

ra to

fi n

d in

g s.

B io

te rr

o ri

sm /

w a

rf a

re s

h o

u ld

b e

sp e

ct e

d if

n u

m e

ro u

s co

ll o

ca te

d c

a su

a lt

ie s

h a

v e

ro g

re ss

iv e

d e

sc e

n d

in g

u lb

a r,

m u

sc u

la r,

a n

re sp

ir a

to ry

w e

a k n

e ss

In tu

b a

ti o

n a

n d

e n

ti la

to ry

a ss

is ta

n ce

r re

sp ir

a to

ry f

a il u

re .

T ra

ch e

o st

o m

y m

a y

b e

q u

ir e

d . A

d m

in is

tr a

ti o

o f

b o

tu li n

u m

a n

ti to

x in

n v

e st

ig a

ti o

n a

l N e

D ru

g [

IN D

] p

ro d

u ct

) m

a y

re v

e n

t o

r d

e cr

e a

p ro

g re

ss io

n t

o r

e sp

ir a

to ry

il u

re a

n d

h a

st e

re co

v e

ry .

P e

n ta

v a

le n

t to

x o

(t y

p e

s A

, B , C

, D , a

n d

E )

is a

v a

il a

b le

a s

a n

I N

p ro

d u

ct f

o r

th o

se a

t h

ig h

sk o

f e

x p

o su

re .

H y

p o

ch lo

ri te

( 0

.5 %

f o

r 10

–1 5

m in

u te

s) a

n d

/o r

so a

p a

n d

w a

te r.

T o

x in

n o

t d

e rm

a ll y

a ct

iv e

n d

s e

co n

d a

ry a

e ro

so ls

re n

o t

a h

a za

rd f

ro m

a ti

e n

ts .

C h

o le

ra In

cu b

a ti

o n

p e

ri o

d is

1 –5

a y

s. A

sy m

p to

m a

ti c

to s

e v

e re

w it

h s

u d

d e

o n

se t.

V o

m it

in g

, a

b d

o m

in a

l d is

te n

ti o

n ,

a n

d p

a in

w it

h li

tt le

r n

o f

e v

e r

fo ll o

w e

ra p

id ly

b y

d ia

rr h

e a

. F

lu id

lo ss

e s

m a

y e

x ce

e d

–1 0

li te

rs p

e r

d a

y .

W it

h o

u t

tr e

a tm

e n

d e

a th

m a

y r

e su

lt f

ro m

v e

re d

e h

y d

ra ti

o n

, h

y p

o v

o le

m ia

, a n

d s

h o

ck .

C li n

ic a

l d ia

g n

o si

W a

te ry

d ia

rr h

e a

a n

d e

h y

d ra

ti o

n . M

ic ro

sc o

p ic

x a

m o

f st

o o

l s a

m p

le s

re v

e a

ls f

e w

o r

n o

r e

o r

w h

it e

c e

ll s.

C a

n b

id e

n ti

fi e

d in

s to

o l b

d a

rk f

ie ld

o r

p h

a se

n tr

a st

m ic

ro sc

o p

a n

d c

a n

b e

g ro

w n

o n

v a

ri e

ty o

f cu

lt u

re m

e d

ia .

F lu

id a

n d

e le

ct ro

ly te

p la

ce m

e n

A n

ti b

io ti

cs s

u ch

a s

te tr

a cy

cl in

e , a

m p

ic il li n

, o

r tr

im e

th o

p ri

m -

su lf

a m

e th

o x a

zo le

w il l

sh o

rt e

n t

h e

d u

ra ti

o n

o f

d ia

rr h

e a

A li

ce n

se d

, k il le

d v

a cc

in e

a v

a il a

b le

b u

t p

ro v

id e

s o

n ly

a b

o u

t 5

0 %

ro te

ct io

n t

h a

t la

st s

n o

o re

t h

a n

6 m

o n

th s.

a cc

in a

ti o

n s

ch e

d u

le is

t 0

a n

d 4

w e

e k s

w it

b o

o st

e r

d o

se s

e v

e ry

m o

n th

P e

rs o

n a

l c o

n ta

ra re

ly c

a u

se s

in fe

ct io

n ;

h o

w e

v e

r, e

n te

ri c

p re

ca u

ti o

n s

a n

d c

a re

fu l

h a

n d

w a

sh in

g s

h o

u ld

b e

e q

u e

n tl

y e

m p

lo y

e d

. B

a ct

e ri

ci d

a l s

o lu

ti o

n s

su ch

a s

h y

p o

ch lo

ri te

o u

ld p

ro v

id e

a d

e q

u a

d e

co n

ta m

in a

ti o

n .

(c o

n ti

n u

e s)

57854_CH09_final.indd 13357854_CH09_final.indd 133 1/20/10 10:29:43 AM1/20/10 10:29:43 AM

F O S T E R , C E D R I C 1 6 9 2 T S

134 Homeland Security: Principles and Practice of Terrorism Response

TA B

LE 9

-1

B io

lo gi

ca l A

ge nt

s: S

ym pt

om s

an d

Tr ea

tm en

t (c

o n

ti n

u e

d )

S ig

n s a

n d s

y m

p to

m s

D ia

g n

o s is

T re

a tm

e n

t P

ro p h

y la

x is

D e c o n

ta m

in a ti

o n

P la

g u

e P

n e

u m

o n

ic p

la g

u e

: In

cu b

a ti

o n

p e

ri o

d is

2 –3

a y

s. H

ig h

f e

v e

r, c

h il ls

, h

e m

o p

ty si

s, t

o x e

m ia

, p

ro g

re ss

in g

r a

p id

ly t

d y

sp n

e a

, s tr

id o

r, a

n d

a n

o si

s. D

e a

th r

e su

lt s

fr o

m r

e sp

ir a

to ry

f a

il u

re ,

ci rc

u la

to ry

c o

ll a

p se

, a n

b le

e d

in g

d ia

th e

si s.

B u

b o

n ic

p la

g u

e :

In cu

b a

ti o

n p

e ri

o d

is 2

–1 0

a y

s. M

a la

is e

, h ig

h f

e v

e r,

n d

t e

n d

e r

ly m

p h

n o

d e

s (b

u b

o e

s) ; m

a y

p ro

g re

sp o

n ta

n e

o u

sl y

t o

t h

se p

ti ce

m ic

f o

rm , w

it h

re a

d t

o t

h e

c e

n tr

a l

n e

rv o

u s

sy st

e m

, l u

n g

a n

d e

ls e

w h

e re

C li n

ic a

l d ia

g n

o si

s. A

re su

m p

ti v

e d

ia g

n o

si s

ca n

b e

m a

d e

b y

G ra

m o

r W

a y

so n

s ta

in o

f ly

m p

n o

d e

a sp

ir a

te s,

s p

u tu

m ,

o r

ce re

b ra

l s p

in a

l f lu

id .

P la

g u

e c

a n

a ls

o b

cu lt

u re

d .

E a

rl y

a d

m in

is tr

a ti

o n

f a

n ti

b io

ti cs

is v

e ry

ff e

ct iv

e . S

u p

p o

rt iv

th e

ra p

y f

o r

p n

e u

m o

n ic

n d

s e

p ti

ce m

ic f

o rm

s is

q u

ir e

d .

A li

ce n

se d

, k il le

d v

a cc

in e

a v

a il a

b le

. I n

it ia

l d o

fo ll o

w e

d b

y a

s e

co n

sm a

ll e

r d

o se

1 –3

m o

n th

s la

te r,

a n

d a

t h

ir d

3 –6

o n

th s

la te

r. A

b o

o st

e r

d o

se is

g iv

e n

a t

6 , 1

2 , a

n d

m o

n th

s, a

n d

t h

e n

e v

e ry

1–

2 y

e a

rs . T

h is

v a

cc in

m a

y n

o t

p ro

te ct

a g

a in

a e

ro so

l e x p

o su

re .

S e

cr e

ti o

n a

n d

le si

o n

re ca

u ti

o n

s w

it h

u b

o n

ic p

la g

u e

s h

o u

b e

p ra

ct ic

e d

. S tr

ic t

is o

la ti

o n

o f

p a

ti e

n ts

it h

p n

e u

m o

n ic

p la

g u

e .

H e

a t,

d is

in fe

ct a

n ts

, a n

e x p

o su

re t

o s

u n

li g

h t

re n

d e

r b

a ct

e ri

a h

a rm

le ss

Q f

e v

e r

F e

v e

r, c

o u

g h

, a n

p le

u ri

ti c

ch e

st p

a in

m a

o cc

u r

a s

e a

rl y

a s

10 d

a y

s a

ft e

r e

x p

o su

re . P

a ti

e n

a re

n o

t g

e n

e ra

ll y

c ri

ti ca

ll y

il l,

a n

d t

h e

il ln

e ss

la st

s fr

o m

2 d

a y

s to

2 w

e e

k s.

Q f

e v

e r

is n

o t

a c

li n

ic a

ll y

is ti

n ct

iv e

il ln

e ss

a n

d m

a y

se m

b le

a v

ir a

l i ll n

e ss

r o

th e

r ty

p e

s o

f a

ty p

ic a

l p

n e

u m

o n

ia . T

h e

d ia

g n

o si

s is

c o

n fi

rm e

d s

e ro

lo g

ic a

ll y

Q f

e v

e r

is g

e n

e ra

ll y

se lf

-l im

it in

g il

ln e

ss e

v e

w it

h o

u t

tr e

a tm

e n

T e

tr a

cy cl

in e

o r

d o

x y

cy cl

in e

a re

t h

tr e

a tm

e n

ts o

f ch

o ic

e a

n d

re o

ra ll y

a d

m in

is te

re d

r 5

–7 d

a y

s. Q

f e

v e

r e

n d

o ca

rd it

is (

ra re

) is

u ch

m o

re d

if fi

cu lt

t o

e a

T re

a tm

e n

t w

it h

tr a

cy cl

in e

d u

ri n

g t

h e

cu b

a ti

o n

p e

ri o

d m

a y

e la

y b

u t

n o

t p

re v

e n

t th

e o

n se

t o

f sy

m p

to m

A n

a ct

iv a

te d

w h

o le

- ce

ll v

a cc

in e

is e

ff e

ct iv

in e

li ci

ti n

g p

ro te

ct io

a g

a in

st e

x p

o su

re , b

u t

se v

e re

lo ca

l r e

a ct

io n

s to

t h

is v

a cc

in e

m a

y b

se e

n in

t h

o se

w h

o a

lr e

a d

p o

ss e

ss im

m u

n it

y .

P a

ti e

n ts

w h

o a

re e

x p

o se

to Q

f e

v e

r b

y a

e ro

so l d

n o

t p

re se

n t

a r

is k f

o r

se co

n d

a ry

c o

n ta

m in

a ti

o n

r re

a e

ro so

li za

ti o

o f

th e

o rg

a n

is m

. D

e co

n ta

m in

a ti

o n

a cc

o m

p li sh

e d

w it

h s

o a

a n

d w

a te

r o

r b

y t

h e

u se

o f

w e

a k (

0 .5

% )

h y

p o

ch lo

ri te

lu ti

o n

57854_CH09_final.indd 13457854_CH09_final.indd 134 1/20/10 10:29:44 AM1/20/10 10:29:44 AM

F O S T E R , C E D R I C 1 6 9 2 T S

CHAPTER 9: Weapons of Mass Effect—Biological Terrorism 135

S ig

n s a

n d s

y m

p to

m s

D ia

g n

o s is

T re

a tm

e n

t P

ro p h

y la

x is

D e c o n

ta m

in a ti

o n

R ic

in W

e a

k n

e ss

, f e

v e

r, c

o u

g h

, a

n d

h y

p o

th e

rm ia

a b

o u

t 3

6 h

o u

rs a

ft e

r a

e ro

so l

e x p

o su

re , f

o ll o

w e

in t

h e

n e

x t

12 h

o u

b y

h y

p o

te n

si o

n a

n d

rd io

v a

sc u

la r

co ll a

p se

S ig

n s

a n

d s

y m

p to

m s

n o

te d

a b

o v

e in

rg e

n u

m b

e rs

o f

g e

o g

ra p

h ic

a ll y

c lu

st e

re d

a ti

e n

ts c

o u

ld s

u g

g e

a n

e x p

o su

re t

a e

ro so

li ze

d r

ic in

. T h

ra p

id t

im e

c o

u rs

e t

se v

e re

s y

m p

to m

s a

n d

e a

th w

o u

ld b

e u

n u

su a

l fo

r in

fe ct

io u

s a

g e

n ts

. L

a b

o ra

to ry

f in

d in

g s

a re

o n

sp e

ci fi

c e

x ce

p t

fo r

sp e

ci fi

c se

ru m

e n

zy m

e -

li n

k e

d im

m u

n o

so rb

e n

t a

ss a

y . A

cu te

a n

co n

v a

le sc

e n

t se

ra s

h o

u ld

e c

o ll e

ct e

d .

P a

ti e

n t

m a

n a

g e

m e

n t

su p

p o

rt iv

e . P

re se

n tl

th e

re is

n o

a v

a il a

b le

n ti

to x in

. G a

st ri

c d

e co

n ta

m in

a ti

o n

e a

su re

s sh

o u

ld b

e m

p lo

y e

d if

t h

e t

o x in

in g

e st

e d

P re

se n

tl y

t h

e re

is n

v a

cc in

e o

r p

ro p

h y

la ct

a n

ti to

x in

a v

a il a

b le

r h

u m

a n

u se

. U se

f a

p ro

te ct

iv e

m a

(r e

sp ir

a to

r) is

c u

rr e

n tl

th e

b e

st p

ro te

ct io

a g

a in

st in

h a

la ti

o n

if a

a tt

a ck

/e x p

o su

re is

n ti

ci p

a te

d .

W e

a k h

y p

o ch

lo ri

so lu

ti o

n s

a n

d /o

r so

a p

a n

w a

te r

ca n

d e

co n

ta m

in a

sk in

s u

rf a

ce s.

R ic

in is

n o

t v

o la

ti le

, s o

s e

co n

d a

a e

ro so

ls a

re g

e n

e ra

ll y

n o

t a

d a

n g

e r

to h

e a

lt h

ca re

ro v

id e

S m

a ll p

o x

C li n

ic a

l m a

n if

e st

a ti

o n

e g

in s

a cu

te ly

w it

m a

la is

e , f

e v

e r,

r ig

o rs

, v

o m

it in

g , h

e a

d a

ch e

, a

n d

b a

ck a

ch e

. A b

o u

t 2

–3 d

a y

s la

te r,

le si

o n

s a

p p

e a

r, w

h ic

h q

u ic

k ly

ro g

re ss

f ro

m m

a cu

le s

to p

a p

u le

s a

n d

e v

e n

tu a

ll y

u st

u la

r v

e si

cl e

s. T

h e

a re

m o

re a

b u

n d

a n

t o

n t

h e

x tr

e m

it ie

s a

n d

f a

ce a

n d

e v

e lo

p s

y n

ch ro

n o

u sl

y .

T e

st s

o f

e le

ct ro

n a

n d

li g

h t

m ic

ro sc

o p

y a

re n

o t

ca p

a b

le o

f d

is cr

im in

a ti

n g

a ri

o la

f ro

m v

a cc

in ia

, m

o n

k e

y p

o x , o

r co

w p

o x .

T h

e la

te st

P o

ly m

e ra

C h

a in

R e

a ct

io n

d ia

g n

o st

ic s

te ch

n iq

u e

s m

a y

b e

m o

a cc

u ra

te in

d is

cr im

in a

ti n

b e

tw e

e n

v a

ri o

la a

n d

o th

e r

O rt

h o

p o

x v

ir u

se s.

A t

p re

se n

t th

e re

is n

e ff

e ct

iv e

c h

e m

o th

e ra

p y

n d

t re

a tm

e n

t o

f a

c li n

ic a

l ca

se r

e m

a in

s su

p p

o rt

iv e

Im m

e d

ia te

v a

cc in

a ti

o n

r re

v a

cc in

a ti

o n

s h

o u

b e

u n

d e

rt a

k e

n f

o r

a ll

p e

rs o

n n

e l e

x p

o se

d .

V a

cc in

ia -i

m m

u n

g lo

b u

li n

is o

f v

a lu

e in

o st

e x p

o su

re p

ro p

h y

la x is

f sm

a ll p

o x w

h e

n g

iv e

w it

h in

t h

e f

ir st

w e

e k

fo ll o

w in

g e

x p

o su

re , a

n d

it h

v a

cc in

a ti

o n

S tr

ic t

q u

a ra

n ti

n e

w it

re sp

ir a

to ry

is o

la ti

o n

f o

r a

m in

im u

m o

f 16

–1 7

d a

y s

fo ll o

w in

g e

x p

o su

re f

o r

a ll

co n

ta ct

s. P

a ti

e n

ts s

h o

u ld

e c

o n

si d

e re

d in

fe ct

io u

s u

n ti

l a ll s

ca b

s se

p a

ra te

(c o

n ti

n u

e s)

57854_CH09_final.indd 13557854_CH09_final.indd 135 1/20/10 10:29:44 AM1/20/10 10:29:44 AM

F O S T E R , C E D R I C 1 6 9 2 T S

136 Homeland Security: Principles and Practice of Terrorism Response

TA B

LE 9

-1

B io

lo gi

ca l A

ge nt

s: S

ym pt

om s

an d

Tr ea

tm en

t (c

o n

ti n

u e

d )

S ig

n s a

n d s

y m

p to

m s

D ia

g n

o s is

T re

a tm

e n

t P

ro p h

y la

x is

D e c o n

ta m

in a ti

o n

S ta

p h

y lo

co cc

a l

e n

te ro

to x in

B F

ro m

3 –1

2 h

o u

rs a

ft e

r a

e ro

so l e

x p

o su

re , s

u d

d e

o n

se t

o f

fe v

e r,

c h

il ls

, h

e a

d a

ch e

, m y

a lg

ia , a

n d

o n

p ro

d u

ct iv

e c

o u

g h

. S

o m

e p

a ti

e n

ts m

a y

e v

e lo

p s

h o

rt n

e ss

o f

b re

a th

a n

d r

e tr

o st

e rn

a l

ch e

st p

a in

. F e

v e

r m

a y

la st

–5 d

a y

s, a

n d

c o

u g

h m

a y

e rs

is t

u p

t o

4 w

e e

k s.

a ti

e n

ts m

a y

a ls

o p

re se

n t

w it

h n

a u

se a

, v o

m it

in g

, a

n d

d ia

rr h

e a

if t

h e

sw a

ll o

w t

h e

t o

x in

. H ig

h e

r e

x p

o su

re le

v e

ls c

a n

le a

to s

e p

ti c

sh o

ck a

n d

d e

a th

C li n

ic a

l d ia

g n

o si

s. P

a ti

e n

t p

re se

n ts

w it

h a

f e

b ri

re sp

ir a

to ry

s y

n d

ro m

w it

h o

u t

ch e

st X

-r a

a b

n o

rm a

li ti

e s.

L a

rg e

u m

b e

rs o

f p

a ti

e n

p re

se n

ti n

g w

it h

t y

p ic

a l

sy m

p to

m s

a n

d s

ig n

s o

f st

a p

h y

lo co

cc a

l e

n te

ro to

x in

B p

u lm

o n

a ry

x p

o su

re w

o u

ld s

u g

g e

a n

in te

n ti

o n

a l a

tt a

ck w

it h

is t

o x in

T re

a tm

e n

t is

li m

it e

d t

su p

p o

rt iv

e c

a re

. A rt

if ic

ia l

v e

n ti

la ti

o n

m ig

h t

b e

e e

d e

d f

o r

v e

ry s

e v

e re

se s

a n

d a

tt e

n ti

o n

t o

u id

m a

n a

g e

m e

n t

e ss

e n

ti a

U se

o f

p ro

te ct

iv e

m a

sk .

T h

e re

is c

u rr

e n

tl y

n o

a cc

in e

a v

a il a

b le

t o

re v

e n

t st

a p

h y

lo co

cc a

l e

n te

ro to

x in

in to

x ic

a ti

o n

H y

p o

ch lo

ri te

( 0

.5 %

f o

r 10

–1 5

m in

u te

s) a

n d

/o r

so a

p a

n d

w a

te r.

D e

st ro

a n

y f

o o

d t

h a

t m

a y

h a

v e

e e

n c

o n

ta m

in a

te d

T ri

ch o

th e

ce n

m y

co to

x in

s (T

2 )

E x p

o su

re c

a u

se s

sk in

a in

, p ru

ri tu

s, r

e d

n e

ss ,

v e

si cl

e s,

n e

cr o

si s,

a n

sl o

u g

h in

g o

f e

p id

e rm

is .

E ff

e ct

s o

n t

h e

a ir

w a

in cl

u d

e n

o se

a n

d t

h ro

a t

p a

in , n

a sa

l d is

ch a

rg e

, it

ch in

g , s

n e

e zi

n g

, c o

u g

h ,

d y

sp n

e a

, w h

e e

zi n

g , c

h e

p a

in , a

n d

h e

m o

p ty

si s.

h e

t o

x in

a ls

o p

ro d

u ce

s e

ff e

ct s

a ft

e r

in g

e st

io n

r e

y e

c o

n ta

ct . S

e v

e re

o is

o n

in g

r e

su lt

s in

ro st

ra ti

o n

, w e

a k n

e ss

, a

ta x ia

, c o

ll a

p se

, s h

o ck

, a

n d

d e

a th

S h

o u

ld b

e s

u sp

e ct

e d

a n

a e

ro so

l a tt

a ck

cc u

rs in

t h

e f

o rm

f y

e ll o

w r

a in

w it

d ro

p le

ts o

f y

e ll o

w f

lu id

n ta

m in

a ti

n g

c lo

th e

s a

n d

t h

e e

n v

ir o

n m

e n

C o

n fi

rm a

ti o

n r

e q

u ir

e s

te st

in g

o f

b lo

o d

, t is

su e

, a

n d

e n

v ir

o n

m e

n ta

l sa

m p

le s.

T h

e re

is n

o s

p e

ci fi

c a

n ti

d o

te . S

u p

e ra

ct iv

ch a

rc o

a l s

h o

u ld

b e

g iv

e n

ra ll y

if s

w a

ll o

w e

d .

T h

e o

n ly

d e

fe n

se is

t o

e a

r p

e rs

o n

a l p

ro te

ct iv

e q

u ip

m e

n t

d u

ri n

g a

a tt

a ck

. N o

s p

e ci

fi c

im m

u n

o th

e ra

p y

o r

ch e

m o

th e

ra p

y is

a v

a il a

b le

r u

se in

t h

e f

ie ld

O u

te r

g a

rm e

n ts

s h

o u

b e

r e

m o

v e

d , a

n d

x p

o se

d s

k in

s h

o u

ld b

d e

co n

ta m

in a

te d

w it

h s

o a

a n

d w

a te

r. E

y e

e x p

o su

sh o

u ld

b e

t re

a te

d b

co p

io u

s sa

li n

e ir

ri g

a ti

o n

. O

n ce

d e

co n

ta m

in a

ti o

n is

m p

le te

, i so

la ti

o n

is n

o t

re q

u ir

e d

57854_CH09_final.indd 13657854_CH09_final.indd 136 1/20/10 10:29:44 AM1/20/10 10:29:44 AM

F O S T E R , C E D R I C 1 6 9 2 T S

CHAPTER 9: Weapons of Mass Effect—Biological Terrorism 137

S ig

n s a

n d s

y m

p to

m s

D ia

g n

o s is

T re

a tm

e n

t P

ro p h

y la

x is

D e c o n

ta m

in a ti

o n

T u

la re

m ia

U lc

e ro

g la

n d

u la

r tu

la re

m ia

p re

se n

ts w

it h

lo ca

l u lc

e r

a n

d r

e g

io n

a l

ly m

p h

a d

e n

o p

a th

y , f

e v

e r,

il ls

, h e

a d

a ch

e , a

n d

a la

is e

. T y

p h

o id

a l o

r se

p ti

ce m

ic t

u la

re m

p re

se n

ts w

it h

f e

v e

h e

a d

a ch

e , m

a la

is e

, su

b st

e rn

a l d

is co

m fo

rt ,

p ro

st ra

ti o

n , w

e ig

h t

lo ss

, a

n d

a n

o n

p ro

d u

ct iv

co u

g h

C li n

ic a

l d ia

g n

o si

P h

y si

ca l f

in d

in g

s a

u su

a ll y

n o

n sp

e ci

fi c.

h e

st X

-r a

y m

a y

v e

a l p

n e

u m

o n

p ro

ce ss

, m e

d ia

st in

a l

ly m

p h

a d

e n

o p

a th

y , o

r p

le u

ra l e

ff u

si o

n . R

o u

ti n

cu lt

u re

is p

o ss

ib le

b u

t d

if fi

cu lt

. T h

e d

ia g

n o

si s

ca n

b e

e st

a b

li sh

e d

b y

ro lo

g y

A d

m in

is tr

a ti

o n

o f

a n

ti b

io ti

cs w

it h

e a

rl y

e a

tm e

n t

is v

e ry

ff e

ct iv

e .

A li

v e

, a tt

e n

u a

te d

a cc

in e

is a

v a

il a

b le

a s

a n

v e

st ig

a ti

o n

a l n

e w

d ru

g .

It is

a d

m in

is te

re d

o n

ce b

sc a

ri fi

ca ti

o n

. A 2

-w e

e k

co u

rs e

o f

te tr

a cy

cl in

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138 Homeland Security: Principles and Practice of Terrorism Response

It is sometimes difficult to distinguish organophos- phate nerve agent poisoning from botulism. The copious secretions of the nerve agent will be the significant clue to the differential. Isolated cases have a wider differential diagnosis including Guillain-Barré syndrome, myasthe- nia gravis, and tick paralysis.

Botulinum toxin penetrates into the cell and blocks release of acetylcholine, preventing neuromuscular trans- mission and leading to muscle weakness and paralysis (Jankovic & Brin, 1991). Botulinum toxin is thought to preferentially affect active neuromuscular fibers and has been shown in rats to have a greater affinity when nerve activity is greater (Hughes & Whaler, 1962). It may also affect the central nervous system (Hallett, Glocker, & Deuschl, 1994). The local injection of botulinum toxin has been used clinically to treat involuntary focal muscle spasms and involuntary dystonia.

Botulinum toxin was used to assassinate Reinhard Heydrich, a Nazi leader and probable successor to Hitler. The Czechoslovakian underground used a gre- nade impregnated with botulinum toxin made by English researchers in Porton Down near Wiltshire, England. Although Heydrich’s wounds were relatively minor, he died unexpectedly several days after the attack (Mobley, 1995). Botulinum is a highly effective weapon of isolated assault. It is a one-shot weapon that is neither commu- nicable or transmittable, but for assignation it can be highly effective.

Detection

Detection of botulinum may be done by mouse bioassay or by liquid chromatography. Uses of radioimmunoas- say and radioreceptor assays have also been reported. A DNA probe has been designed for detection of botulinum toxin, which would markedly expedite diagnosis. An immunoassay has been developed by Environmental Technologies Group, Incorporated, in Baltimore, Maryland, to detect this toxin, ricin, and staphylococ- cal enterotoxin.

Survivors will probably not develop an antibody response due to the small amount of toxin required for lethality.

Prophylaxis and Treatment

Botulinum toxoid vaccine is available (Hanson, 1994; Hatheway, 1995; Wiener, 1996). The CDC provides a pentavalent vaccine that gives protection from toxin types A, B, C, D, and E but provides no protection against the F and G type toxins. The military believes that F and G type toxins are unlikely to be used in warfare because the strains of Clostridium botulinum that produce toxins F and G are difficult to grow in large quantities. If new techniques allow production of toxins F and G

in large quantities, the pentavalent vaccine will be use- less. A heptavalent antitoxin against types A through G is available in limited supply at the U.S. Army Medical Research Institute of Infectious Diseases in Fort Detrick, Frederick, Maryland.

Treatment is supportive. Respiratory failure will require prolonged (weeks to months) ventilatory sup- port. If ventilatory support is available, fatalities are likely to occur in less than 5 percent of the exposed population.

An equine antitoxin is available and may be of some help in both food-borne and aerosol botulism. This is available from the CDC and protects against A, B, and E toxins. It has been used for treating ingestion botulism and should be given as soon as the diagnosis is made. It is not without its own risks and it does not reverse paralysis, but does prevent progression of the disease. There is no human-based antitoxin currently available, but human- based antitoxin testing is now in progress. Obviously, it will not help in types C and D intoxication.

Although penicillin has been recommended, it is controversial because it may increase the release of toxin in the gut and may worsen neurological symp- toms through lysis of bacterial cells in the gut or wound (Hatheway, 1995). It is also assumed to be ineffective if the toxin were to be inhaled in a direct toxin release.

Clostridium Toxins Tetanus neurotoxin is secreted by Clostridium species in similar fashion to botulinum. The toxin is a single 150,000-dalton polypeptide that is cleaved into two pep- tides held together by disulfide and noncovalent bonds. The intoxication occurs at extremely low concentrations of toxin, is irreversible, and, like botulism, affects the activity of the nerve cell when toxicity occurs.

Clostridium perfringens also secretes at least 12 toxins and can produce gas gangrene (clostridial myonecrosis), enteritis necroticans, and clostridium food poisoning. One or more of these toxins could be produced as a weapon. The alpha toxin is a highly toxic phospholipase that could be lethal when delivered as an aerosol.

Clinical Effects

Where botulinum toxin causes a flaccid paralysis, tetanus causes spastic paralysis. The tetanus neurotoxin migrates retroaxonally (up the nerve fiber) and by transcytosis, it reaches the spinal inhibitory neurons, where it blocks neurotransmitter release and thus causes a spastic pa- ralysis. Despite the seemingly different actions of tetanus and botulism, the toxins act in a similar way at the ap- propriate cellular level. The clinical effect in humans is well documented and includes twitches, spasms, rictus sardonicus, and convulsions.

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Clostridium perfringens alpha toxin would cause vascular leaks, pulmonary damage, thrombocytopenia, and hepatic damage. In the case of an inhaled clostrid- ium perfringens, severe respiratory distress would occur rapidly.

Detection

If C. perfringens is suspected, acute serum and tissue samples should be collected for further testing. Specific immunoassays are available for both C. perfringens and C. tetani species. As with most of these toxins and dis- eases, specific laboratory findings may be too late to be of clinical use.

Prophylaxis and Treatment

C. perfringens and tetanus are generally sensitive to penicillin, and this is the current drug of choice. There are some data that indicate treatment with either clin- damycin or rifampin may decrease C. perfringens toxin production and give better results.

Every medical provider is aware of the schedule for tetanus immunizations. It is unlikely that there will be any use of this toxin in the United States due to wide- spread tetanus immunization (Lebeda, 1997).This may not be true in other countries, and in the United States there has been no published program about clinical syndromes of overwhelming amounts of tetanus toxin. Although the U.S. military apparently discounts this toxin, it is so easy to make and spread and so lethal that it would make a useful biological toxin.

There is no specific prophylaxis against most of the C. perfringens toxins. Some toxoids for enteritis necroti- cans are available for humans. Veterinary toxoids are in wide use.

Ricin Ricin is a type II ribosome inactivating protein produced by the castor bean plant and secreted in the castor seeds (CP FIGURE 9-1). The toxin is a 576 amino acid protein precursor weighing 65,000 daltons. Once inside the cell, ricin depurinates an adenine from rRNA and thereby inactivates the ribosome, killing the cell.

Ricin is available worldwide by simple chemical pro- cess of the castor bean. Although ricin is only a natural product of the castor bean plant, ricin has been produced from transgenic tobacco using gene transfer principles. Large amounts of toxin could not be produced easily by this transgenic method (Sehnke, Pedrosa, & Paul, Frankel, & Ferl 1994).

Clinical Effects

The clinical picture of ricin poisoning depends on the route of exposure. Castor bean ingestion causes rapid onset of nausea, vomiting, abdominal cramps, coughing

up blood, seizure activity, and severe diarrhea followed by vascular collapse. Death usually occurs on the third day. Inhalation of ricin will cause nonspecific weakness, cough, fever, hypothermia, and hypotension, followed by cardiovascular collapse about 24 to 36 hours after inhalation. Death will occur about 36 to 48 hours after inhalation. High doses by inhalation appear to produce severe enough pulmonary damage to cause death.

At least one fatality has been documented as a di- rect result of ricin employed in biowarfare. In 1978, ricin-impregnated pellets were fired from an umbrella at Georgi Markov and Vladimir Kostov. The pellets were coated with wax designed to melt at body temperature and release the ricin. Markov died as a result of the ricin attack, but Kostov survived. At least six other as- sassinations have used the same technique, according to intelligence sources.

Detection

Enzyme-linked immunosorbent assay for blood or his- tochemical analysis may be useful in confirming ricin intoxication. Ricin causes marked immune response and sera should be obtained from survivors for measurement of antibody response. An immunoassay technique has been developed by Environmental Technologies Group for ricin.

Standard laboratory tests are of little help in diag- nosis of ricin intoxication. The patient may have some leukocytosis with neutrophil predominance. The pleo- morphic picture of ricin intoxication would suggest many respiratory pathogens and may be of little help in diagnosis.

Prophylaxis and Treatment

There is no approved immunologic treatment or chemo- prophylaxis for ricin poisoning at this time. Respiratory protection will prevent inhalation exposure and is the best prophylaxis currently available. Ricin has no dermal activity and is not transported through the skin.

There is ongoing effort to produce both active im- munization and passive antibody prophylaxis suitable for humans. These techniques have been used in animals.

Treatment is supportive and includes both respira- tory support and cardiovascular support as needed. If oral ingestion is suspected, lavage followed by charcoal is appropriate.

Saxitoxin Saxitoxin is a dinoflagellate toxin responsible for para- lytic shellfish poisoning. It is also found in several species of puffers and other marine animals and was originally discovered in 1927 (Sato et al., 1997). The toxin is very soluble in water, is heat stable, and is not destroyed by

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140 Homeland Security: Principles and Practice of Terrorism Response

cooking. The lethal dose is 1 to 2 mg. There are multiple related toxins with substitutions at key positions.

Clinical Effects

Saxitoxin is similar in effects and treatment to tetrodo- toxin. Onset of symptoms is within minutes of exposure. Death may occur within 24 hours. If the patient survives, normal functions are regained within a few days.

Detection

A mouse unit is the minimum amount of saxitoxin that will kill a 20-gram mouse within 15 minutes. There is a standardized mouse assay for routine surveillance, and immunoassays are available.

Prophylaxis and Treatment

There is no antidote for saxitoxin, so symptomatic treat- ment is appropriate. Antibodies for tetrodotoxin will frequently protect against saxitoxin (Kaufman, Wright, Ballou, & Monheit, 1991).

Staphylococcal Enterotoxin Staphylococcal food poisoning is familiar to most emer- gency practitioners. Although the disease is changed when the enterotoxin is delivered via aerosol, it will result in the common food poisoning syndrome. The organism that produces this agent is readily available and could be tailored to produce large quantities of the toxin.

Clinical Effects

Staphylococcal food poisoning begins 1 to 6 hours after exposure with the sudden onset of fever, chills, head- ache, myalgias, and a nonproductive cough. The cough may progress to dyspnea and substernal chest pain. In severe cases, pulmonary edema may be found. Nausea, vomiting, and diarrhea are common (as in the poisoning familiar to emergency physicians). The only physical finding of note is conjunctival injection.

In food-borne staphylococcal enterotoxin B, fever and respiratory involvement are not found, and the gastrointestinal symptoms predominate. Sickness may last as long as 2 weeks and severe exposures may cause fatalities.

Detection

The lab is not helpful in diagnosing staphylococcal en- terotoxin poisoning. Erythrocyte sedimentation rate may be elevated, but this is a nonspecific finding. A chest X-ray is usually normal, but it may have increased interstitial markings and possibly pulmonary edema. An immunoassay has been developed by Environmental Technologies Group from Baltimore, Maryland, that is cost efficient and usable in the field environment.

Prophylaxis and Treatment

There is no significant treatment regimen available for staphylococcal enterotoxin. Therapy is entirely support-

ive. There is no current prophylaxis available, although experimental immunization has been reported.

Tetrodotoxin Tetrodotoxin is a potent neurotoxin produced by fish, salamanders, frogs, octopus, starfish, and mollusks, no- tably the puffer (also called the globefish or blowfish) (Lange, 1990).The dangers of tetrodotoxin poisoning were known by the ancient Egyptians (2400 to 2700 B.C.). All organs of the freshwater puffer are toxic with the skin having the highest toxicity followed by gonad, muscle, liver, and intestine. In saltwater puffers, the liver is the most toxic organ. The lethal dose of tetrodotoxin is only 5 micrograms per kilogram in the guinea pig.

Puffer intoxication is a serious public health problem in Japan, and over 50 people each year are intoxicated. Raw puffer fish, commonly called fugu, is a delicacy in several Southeast Asian countries including Japan. Consumption of fugu causes mild tetrodotoxin intoxi- cation with a pleasant peripheral and perioral tingling sensation. Improperly prepared fugu may contain a le- thal quantity of tetrodotoxin. Fatalities have gradually decreased because of the increased understanding of the toxin and careful preparation of the puffer for food (Laobhripatr et al., 1990). Cooking the food will not dissipate the toxin. Tetrodotoxin is heat stable.

There are several microbial sources of tetrodotoxin including Pseudomonas, Vibrio, Listonella, and Alteromonas species. Although there is only one known bacteria that has produced tetrodotoxin toxicity in humans, there is a significant potential for genetic alteration of common species of bacteria to produce tetrodotoxin (Nozue et al., 1990).

Tetrodotoxin is well known for its ability to inhibit neuromuscular function by blocking the axonal sodium channels (Tambyah, Hui, Gopalakrishnakone, & Chin, 1994). Mortality from tetrodotoxin is thought to be due to hypoxic brain damage from prolonged respiratory paralysis.

Clinical Effects

The clinical symptoms and signs of tetrodotoxin poi- soning are similar to those of the acetylcholinesterase poisons (Mackenzie, Smalley, Barnas, & Park, 1996). Clinical symptoms include nausea, vomiting, vertigo, perioral numbness, unsteady gait, and extremity numb- ness. Clinical symptoms begin within 30 minutes of in- gestion. The speed of onset depends on the quantity of the toxin ingested. The symptoms progress to muscle weakness, chest tightness, diaphoresis, dyspnea, chest pain, and finally paralysis. Hypotension and respira- tory failure are seen in severe poisonings. Patients will frequently complain of a sensation of cold or chilliness.

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Paresthesias spread to the extremities with symptoms often more pronounced distally. Death can occur within 17 minutes after ingestion of tetrodotoxin.

Detection

Detection of tetrodotoxin is by mouse bioassay (Yasumoto, 1991) or by liquid chromatography. Use of radioimmu- noassay and radioreceptor assays has also been reported. An in vitro colorimetric cell assay against a rabbit an- tiserum has been developed and may be more rapid than older methods, but it is not yet publicly available (Kaufman et al., 1991).

Prophylaxis and Treatment

At present, there is no known antidote for tetrodotoxin intoxication. There are numerous anecdotal treatments of survivors with supportive therapy alone. Certainly respiratory support and airway management will be life- saving for a majority of these patients. Gastric lavage will remove unabsorbed toxin from the gut and is used in puffer fish intoxication. Activated charcoal has been reported to effectively bind the toxin and may be em- ployed in ingestions.

4-Aminopyridine has been used to treat tetrodotoxin intoxication in laboratory animals (Chang et al., 1996). 4-Aminopyridine is a potent potassium channel blocker and enhances impulse evoked acetylcholine release from presynaptic motor terminals. There have been no hu- man studies of its use as an antidote. 4-Aminopyridine can cause muscle fasciculation and seizures in a dose- dependent phenomenon.

Naloxone has been proposed as a possible antidote against tetrodotoxin intoxication, because the opiates and tetrodotoxin have similar molecular configurations (Sims & Ostman, 1986). There are no reports of this in either laboratory or clinical use.

Active and passive immunization against tetrodotoxin has been demonstrated in laboratory animals, although there is no known available human immunization for tet- rodotoxin (Fukiya & Matsumura, 1992). Tolerance does not develop on repeated puffer fish exposure. Monoclonal antibodies have been produced and protected laboratory animals against lethal doses of tetrodotoxin (Matsumura, 1995; Rivera, Poli, & Bignami, 1995).

Trichothecene Mycotoxins The trichothecene mycotoxins are produced by fungi and achieved fame in the 1970s as the best candidates for the infamous yellow rain found in Laos, Cambodia, and Afghanistan. Naturally occurring trichothecenes have caused moldy corn toxicosis in animals.

Trichothecene mycotoxins are potent inhibitors of protein synthesis, inhibit mitochondrial respiration, im- pair DNA synthesis, and destroy cell membranes.

Clinical Effects

Consumption of trichothecenes causes weight loss, vomiting, bloody diarrhea, and diffuse hemorrhage. The onset of the illness occurs within hours, and death occurs within 12 hours. Inhalation adds respiratory dis- tress and failure to the picture. Survivors have reported a radiation-sickness-like disease. This has included fe- ver, nausea, vomiting, leukopenia, diarrhea, bleeding, and finally sepsis. Painful skin lesions also occur in survivors.

Detection

There is no readily available diagnostic test for trichoth- ecenes, although reference laboratories may be able to help with gas-liquid chromatography. There are some polyclonal and monoclonal antibodies for detection in liquid or solid samples. Urine samples are most useful for this purpose because the metabolites can be detected as long as 28 days after exposure to the agent.

Prophylaxis and Treatment

Ascorbic acid has been proposed to decrease the lethal- ity of trichothecenes. This has been studied in animals only, but because ascorbic acid has few side effects and is cheap, it should be used in all suspected cases.

Dexamethasone (1 to 10 mg intravenously) has also been shown to decrease lethality as late as 3 hours after exposure to these toxins.

In ingestions, charcoal or superactivated charcoal will absorb remaining toxin and decrease lethality.

Possible Live Bacteriological Warfare Agents

Possible live bacteriological warfare agents include only a few diseases that have been researched. Much of the information that is known to those in the field was obtained from The United States Army Field Manual 8–9; Handbook on the Medical Aspects of NBC Defensive Operations (FM 8–9) (U.S. Army, 1996; also available on the Internet at http://www.nbc-med.org/FMs). Other diseases have been proposed and researched as a result of multiple sessions with interested colleagues and this author’s travels to the city of Sverdlovsk in the Union of Soviet Socialist Republics.

Although these diseases have been proposed by the U.S. military and others as possible biological war- fare agents, there is no question that the list is neither exhaustive nor all-inclusive. Other diseases that have been considered include typhoid fever, Ebola virus, melioidosis, Rift Valley fever, epidemic typhus, Rocky Mountain spotted fever, scrub typhus, coccidiomyco- sis, histoplasmosis, Chikun-Gunya fever, Crimean- Congo fever, Lassa fever, dengue fever, eastern equine

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encephalitis, western equine encephalitis, Venezuelan encephalitis, Omsk hemorrhagic fever, Korean hemor- rhagic fever, and many others (at least 60). The astute reader can recognize the potential for biowarfare in almost any disease that can possibly afflict humans. Numerous other diseases could be used as biowarfare agents against selected crops or livestock.

With the current level of gene manipulation, it is easy to foresee a chimera-tailored bacteria or rickett- sia that has characteristics of one disease, with tailored resistance to all usual antibiotics, yet responsive to an unusual antibiotic that the designer has stockpiled. It is equally easy to think of a tailored virus that has un- usual mortality for white Anglo-Saxon males, but has little mortality for Asian or African American people. One does not have to imagine an increase in lethality in order to find substantial biowarfare applications. A rapidly spreading upper respiratory illness—the com- mon cold—that merely causes 3 days of cough, fever, rhinorrhea, and malaise could be incapacitating if an entire army caught it simultaneously. A city’s police force would be unable to deal with terrorists effectively if over three-fourths of the entire city’s population had uncon- trollable diarrhea for a 2- or 3-day course.

Anthrax Anthrax is caused by Bacillus anthracis. Under usual (nonwartime) conditions, humans become infected by contact with an infected animal or contaminated ani- mal by-products. Anthrax is also known as wool-sorter’s disease. This refers to the sheep shearers of the United Kingdom who frequently get the cutaneous form of the disease as part of the wool production process. There are three forms of anthrax: cutaneous, inhalation, and gastrointestinal. Almost all naturally occurring cases of anthrax are cutaneous or gastrointestinal.

Anthrax was proposed and investigated as a bio- weapon by both the Allies in World War II and the Communists in the former Union of Soviet Socialist Republics. Indeed, an epidemic that caused 96 cases of human anthrax in the city of Ekatrinburg (formerly Sverdlosvk) in the spring of 1979 has been traced to an escaped Russian BW strain of anthrax. In these pa- tients, the pathogen was airborne. Although medical records were confiscated by the Soviet State Security Committee known as the KGB, investigators have pieced together the epidemiology and the source of the epi- demic (Meselson et al., 1994). Following the epidemic, thousands of citizens were immunized against anthrax, the exteriors of the buildings and trees were washed by local fire brigades, and several unpaved streets were asphalted. Notably absent in the public health response

was a military component. In 1992, Russian President Boris Yeltzin admitted that the military was the source of the outbreak. Perestroika and the downfall of the former Communist empire has led to greater release of information, but the staff of city hospital number 40, where the victims were cared for, remains quite sensitive in discussions about this event (Maniscalco, 2001).

In the case of weaponization of anthrax, it is likely to be disseminated as an aerosol of the very persistent spores. The incubation time is from 1 to 6 days, but as the Ekatrinburg incident showed, anthrax may have a prolonged incubation period of up to 2 months. The longer incubation periods are seen most frequently when partial treatment has been given. The spores can be quite stable, even in the alveolus, and as such frequently re- main dormant, but very much alive for up to 3 months. The duration of the disease is between 2 and 5 days.

Presentation

The inhalation form of anthrax is particularly uncom- mon and particularly lethal. In its early presentation, inhalation anthrax could be confused with a plethora of viral or bacterial respiratory illnesses. The disease pro- gresses over 2 to 3 days acting much like a common flu and then suddenly develops respiratory distress, shock, and death within 36 hours. Widening of the mediasti- num on chest radiograph is common in the later stages of the disease and is due to the swollen and engorged lymph nodes within the mediastinum. Unfortunately the radiographic evidence is a late finding and does not bode well for survival of the patient. Evidence of infiltrates on the chest X-ray are uncommon. Other suggestive findings include chest wall edema, hemorrhagic pleural effusions, and hemorrhagic meningitis.

Diagnosis

Diagnosis can be made by culture of blood, pleural fluid, or cerebrospinal fluid. The blood culture is most often positive. In fatal cases, impressions of mediastinal lymph nodes or spleen will be positive. Anthrax toxin may be detected in blood by immunoassay.

The cases in Ekatrinburg were diagnosed on autopsy by a pathologist who noted a peculiar “cardinal’s cap” meningeal inflammation typical in anthrax. Inhalational anthrax may be diagnosed at autopsy by the mediastinal inflammation that can also be observed on computerized tomography scan of the chest in the living patient.

Environmental Technologies Group, Incorporated, has developed an immunoassay for anthrax.

Therapy

Penicillin is considered the drug of choice for treatment of naturally occurring anthrax. However, penicillin- resistant strains do exist, and one could expect that

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anthrax used for a BW would be developed as peni- cillin resistant. Tetracycline and erythromycin have been used for patients who are allergic to penicillin. Induction of resistance to these antibiotics is an easy exercise for genetic manipulation, and warfare strains should be presumed to be resistant to these antibiotics until proven otherwise. Chloramphenicol, gentamycin, and ciprofloxacin would be appropriate choices for ini- tial therapy. The U.S. military recommends oral cipro- floxacin or intravenous doxycycline for initial therapy (U.S. Army, 1996). This therapy is not appropriate for those under 18 years of age or for pregnant females. Supportive therapy for airway, shock, and fluid volume deficits is appropriate.

Prophylaxis

Two types of anthrax vaccine for human use are avail- able in the United States and United Kingdom, albeit in totally insufficient quantities for a civilian biological warfare challenge. Both are based on the partially puri- fied protective antigen of the Bacillus anthracis adsorbed to an aluminum adjuvant. The usual immunization se- ries is six 0.5 mL doses over a span of 18 months. The military feels that a primary series of three 0.5 mL doses (at 0, 2, and 4 weeks) will be protective against both cutaneous and inhalation anthrax for about 6 months after the primary series. These immunizations were given to many coalition troops during the Gulf War in anticipation of Saddam Hussein’s employment of this agent. Large quantities of antigen are presumed to be stockpiled for military use because this agent has been a recurring threat. Unless civilian immunizations start about 1 month prior to a terrorist attack, EMS and medi- cal providers will be essentially unprotected.

Although minor reactions to the anthrax vaccine are common (occurring in 6 percent of the immunized population), major reactions are uncommon. Obviously, the vaccine is contraindicated for those who are known to be sensitive to it and for those who have already had clinical anthrax. The choice between immunization and some allergic reaction and no immunization in the face of a serious biowarfare threat presents a difficult clinical dilemma.

Live anthrax vaccine is used in Russia to immunize both livestock and human beings. It is a spore vaccine with both STI-1 and strain 3 mixtures. The Russians feel that this vaccine is superior at stimulating cell-mediated immunity (Shlyakhov & Rubinstein, 1994). There would be considerable resistance to use of the Russian vaccine in Western countries because of concerns over purity and residual virulence of a live vaccine.

There is no available evidence that these vaccines will adequately protect against an aerosol challenge. New

vaccines with a highly purified protective antigen or designer attenuated strains have both been used in labo- ratories but are not commercially available (Coulson, Fulop, & Titball, 1994; Ivins et al., 1995).

Antibiotic prophylaxis with ciprofloxacin (500 mg orally twice day), or doxycycline (100 mg orally twice a day) is also recommended by the U.S. military for an im- minent attack by a BW. Should the attack be confirmed as anthrax, then antibiotics should be continued for 4 weeks for all who are exposed. Those exposed should also be started on antianthrax vaccine with the standard schedule (if it is available) if they have not been previ- ously immunized. Those who have received fewer than three doses of vaccine prior to exposure should receive a single booster injection. If vaccine is not available, an- tibiotics should be continued until patients can be safely and closely observed when the antibiotics are discon- tinued. Inhaled spores are not destroyed by antibiotics and may persist beyond the course of recommended antibiotics.

Brucellosis Brucellosis is a zoonotic disease caused by small non- motile coccobacilli. The natural reservoir is domestic herbivores such as goats, sheep, cattle, and pigs. There are four species: Brucella melitensis, B. abortus (cattle), B. suis (pigs), and B. canis (dogs). Humans become in- fected when they ingest raw infected meat or milk, inhale contaminated aerosols, or make contact with their skin. Human infection is also called undulant fever. Human- to-human transmission can occur only if serum is passed from an infected patient to another human, so it is ex- tremely rare.

Brucella species have been long considered as bio- logical warfare agents because of the stability, persis- tence, and ease of infection without human-to-human transfer. Brucellosis can be spread by aerosol spray or by contamination of food supply (sabotage). There is a long persistence in wet ground or food.

Presentation

The incubation period for brucellosis is about 8 to 14 days, but may be considerably longer. Clinical disease is a nonspecific febrile illness with headache, fatigue, myalgias, anorexia, chills, sweats, and cough. The fe- ver can reach up to 105°F. The disease may progress and include arthritis, lymphadenopathy, arthralgias, osteomyelitis, epididymitis, orchitis, and endocarditis. Disability is pronounced, but lethality is only about 5 percent or less in usual cases. The disease may be followed by recovery and relapse. The duration of the disease is usually a few weeks, but brucellosis can last for years.

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Diagnosis

Diagnosis of brucellosis is by blood culture, by bone marrow culture, or by serology. There are no other laboratory findings that contribute to a diagnosis of brucellosis.

Therapy

To treat brucellosis, the U.S. military recommends doxy- cycline (100 mg twice a day) plus rifampin (900 mg/day) for 6 weeks. These antibiotics are generally available in sufficient quantities in the United States. Alternative proposed therapy has been doxycycline (100 mg twice a day) for 6 weeks and streptomycin (1 g/day) for 3 weeks. Trimethoprim/sulfamethoxazole has been given for 4 to 6 weeks but is thought to be less effective. Relapse and treatment failure is common.

Prophylaxis

There is no information available about chemoprophy- laxis for brucellosis. Human vaccines are not routinely available in the United States, but they have been devel- oped by other countries. A variant of B. abortus, S19-BA, has been used in the former Union of Soviet Socialist Republics to protect occupationally exposed groups. Efficacy is limited and annual revaccination is needed. A similar vaccine is available in China. Neither of these two vaccines would meet Western requirements for safety and effectiveness (Corbel, 1997).

Cholera Cholera is a well-known diarrheal disease caused by Vibrio cholerae acquired in humans through ingestion of contaminated water. The organism causes a pro- found secretory rice-water diarrhea by elaborating an enterotoxin.

Although cholera can be spread by aerosols, more likely terrorist or military employment would be con- tamination of food or water supplies. There is negligible direct human-to-human transmissibility. The bacterium does not have long persistence in food or pure water and is not persistent when applied by aerosols, thereby mak- ing it an ineffective bioweapon for mass distribution.

Presentation

Cholera can cause a profuse, watery diarrhea that causes hypovolemia and hypotension. Without treat- ment, cholera can rapidly kill adults and children alike from severe dehydration and resultant shock. The in- cubation period is 1 to 5 days and the course of the illness is about 1 week.

A patient with cholera may have vomiting early in the illness. There is little abdominal pain associated with the disease. The hallmark of the disease is rice-water diarrhea.

Diagnosis

Gram staining of the stool sample of a person with cholera will show few or no red or white cells. Renal failure may complicate severe dehydration. Electrolyte abnormalities are common with the profound fluid loss; generally hypokalemia predominates.

Rotavirus, Escherichia coli, and toxic ingestions such as staphylococcal food poisoning, Bacillus cereus, and even clostridia species can cause similar watery diar- rhea. Bacteriological diagnosis of cholera diarrhea has been well studied for decades. Vibrio species can be seen and identified readily with dark field or phase contrast microscopes. Culture will prove the diagnosis but is not necessary for the treatment.

Therapy

Treatment of cholera is mostly supportive. Although most U.S. emergency physicians are used to treating significant hypovolemia with intravenous fluid re- placement, it is unlikely to be readily available if an epidemic of cholera is caused by terrorist or enemy action. The World Health Organization (WHO) oral rehydration formula is appropriate but generally not stocked in sufficient quantities in most cities. Pedialyte and sport drinks such as Gatorade will provide interim oral hydration. If a cholera epidemic develops, intra- venous fluids should be reserved for those patients who are vomiting and cannot tolerate oral rehydration, patients who have more than 7 liters per day of stool, and patients who have extensive hypovolemia and are in clinical shock.

Tetracycline and doxycycline have both been found to shorten the course of the diarrhea. Other effective drugs include ampicillin (250 mg every 6 hours for 5 days) and trimethoprim/sulfamethoxazole (1 tablet every 12 hours). Appropriate alteration of dosages should be used for pediatric patients.

Prophylaxis

The currently available vaccine for cholera is a killed sus- pension of V. cholerae. It provides incomplete protection and lasts for no longer than 6 months. It requires two injections with a booster dose every 6 months. Improved vaccines are being tested but are not yet available.

Ebola Virus The Ebola virus is a member of a family of RNA viruses known as filoviruses commonly referred to as viral hem- orrhagic fever (VHF) (CP FIGURE 9-2). When magnified several thousand times by an electron microscope, these viruses have the appearance of long filaments or threads. Ebola virus was discovered in 1976 and was named for a river in Zaire, Africa, where it was first detected (CDC, 2009).

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Ebola virus has been covered significantly in the pop- ular literature and in several books and movies (including Outbreak). Members of the Aum Shinrikyo cult visited Zaire to collect Ebola. This virus is highly contagious and easily spread by body fluids, particularly blood. It is quite dangerous for the healthcare provider because human- to-human contact will rapidly spread the disease. Ebola and all of the VHFs are capable of being aerosolized.

Use of this virus (with greater than 90 percent le- thality) would be considered a doomsday operation by the military. There is no guarantee that this virus would be able to be contained if spread to a modern city. The persistence is low, but the transmissibility is so high that this is immaterial.

For example, the distribution of the virus might be effective by simply putting an infected individual on a plane that flies around the world and ensuring that he coughs repeatedly. The effect of this distribution plan could be extraordinary because the incubation period for overt illness is upwards of 14 days.

Presentation

Ebola virus is a viral hemorrhagic fever. It can be spread by blood and blood products, secretions, and by drop- let nuclei or aerosol transmission ( Jaax et al., 1995). It is highly lethal (more than 90 percent) with a rapid course.

Diagnosis

A diagnosis is made by detection of Ebola antigens, anti- body, or genetic material, or by culture of the virus from these sources. Diagnostic tests are usually performed on clinical specimens that have been treated to inactivate (kill) the virus. Research on Ebola virus must be done in a special, high-containment laboratory to protect sci- entists working with infected tissues.

Therapy

Therapy is supportive only and involves extensive critical care medicine including artificial ventilation. A release of Ebola would significantly tax the overall healthcare sys- tem and require tremendous resources for each patient. Even then it is important that everyone understand that there is no known therapy for this disease.

Prophylaxis

There is no known prophylaxis for Ebola virus. Sera from survivors have been obtained, and it is possible that passive protection could be developed. A recent accidental exposure to live Ebola virus was successfully treated with convalescent antisera.

Plague Plague is a zoonotic disease caused by Yersinia pestis. It is naturally found on rodents and prairie dogs and

their fleas. Under normal conditions, the following three syndromes are recognized: inhalational (pneumonic), septicemic, and bubonic. Usually an initial infection is in the form of bubonic plague.

In 1994 defectors revealed that the Russians had conducted research on Yersinia pestis, the plague bac- terium, to make it more virulent and stable in the environment. The plague can retain viability in water for 2 to 30 days, in moist areas for up to 2 years, and in near freezing temperatures for several months to a year.

Plague could be spread by either infected vectors such as fleas or by an aerosol spray. Person-to-person transmissibility is high and the bacterium is highly in- fective. The persistence is low, but the transmissibility is so high that this is immaterial.

Presentation

In bubonic plague, the incubation period is from 2 to 10 days. The onset is acute with malaise, fever (often quite high), and purulent lymphadenitis. The lymphadenitis is most often inguinal, but cervical and axillary nodes can also be involved, depending on where the flee bites occurred (CP FIGURE 9-3A and CP FIGURE 9-3B). As the disease progresses, the nodes become tender, fluctuant, and fi- nally necrotic. The bubonic form may progress to the septicemic form whereby the plague bacterium infects the major organ systems systemically. Involvement of the lungs results in the pneumonic form and the patient be- comes contagious through coughing and droplet nuclei. The course of the disease is 2 to 3 days, and the disease has a high mortality rate.

In primary pneumonic plague, the incubation pe- riod is 2 to 3 days. The onset is acute and fulminant with malaise, fever, chills, cough with bloody sputum, and toxemia. The pneumonia progresses rapidly to respira- tory failure with dyspnea, stridor, and cyanosis.

In untreated patients, the mortality is over 50 percent for the bubonic and septicemic forms. In the pneumonic form, the mortality approaches 100 percent. The termi- nal events in septicemic plague are circulatory collapse, hemorrhage, and peripheral thrombosis. In pneumonic plague, the terminal event is often respiratory failure as well as circulatory collapse.

Diagnosis

A presumptive diagnosis of plague can be made by find- ing the typical safety pin bipolar staining organisms in Giemsa-stained specimens. Appropriate specimens are lymph node aspirate, sputum, or cerebral spinal fluid. Immunofluorescent staining is available and helpful if readily accessible. Y. pestis can be readily cultured from any of these sources.

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Environmental Technologies Group, Incorporated, has developed an immunoassay for plague.

Therapy

Plague is readily contagious and strict isolation of patients is essential. Streptomycin, tetracycline, and chloram- phenicol are all useful if they are given within the first 24 hours after symptoms of pneumonic plague begin. Supportive therapy of complications is essential.

Prophylaxis

Plague vaccine is available but has not been shown to be effective against an aerosol exposure and subsequent pneumonic plague. The plague vaccine is a whole cell formalin-killed product. The usual dose is 0.5 mL given at 0, 1, and 2 weeks.

Plague vaccines providing protection against aerosol exposure are not yet available but are under develop- ment (Oyston et al., 1995). Current whole-cell plague vaccines stimulate immunity against the bubonic form but are probably not effective for the pneumonic form (Meyer, 1970; Russel et al., 1995).

Q Fever Q fever is a rickettsial zoonotic disease caused by Coxiella burnetii. The usual animals affected are sheep, cattle, and goats. Human disease is usually caused by inhalation of particles contaminated with Coxiella.

Presentation

Q fever is a self-limiting febrile illness of 2 days to 2 weeks. The incubation period is about 10 to 20 days. The patient is visually ill, but uneventful recovery is the rule. Q fever pneumonia is a frequent complication and may be noted only on radiographs in most cases. Some patients will have nonproductive cough and pleuritic chest pain. Other complications are not common and may include chronic hepatitis, endocarditis, meningitis, encephalitis, and osteomyelitis.

The value of this disease as a BW is in disruption of society. Mass distribution of the C. burnetii would cause significant societal disruption by overloading the healthcare system, creating fear, and causing mass social distancing, thereby disrupting the economy.

Diagnosis

Q fever’s presentation as a febrile illness with an atypical pneumonia (characterized by a dry cough) is similar to a host of other atypical pneumonias, including myco- plasma, legionnaire’s disease, chlamydia pneumonia, psittacosis, or hantavirus.

The diagnosis can be confirmed serologically and other laboratory findings are unlikely to be helpful. Most

patients with Q fever will have slightly elevated liver enzymes. It is difficult to isolate rickettsia, and Q fever is no exception.

Therapy

As with other rickettsial diseases such as Rocky Mountain spotted fever, the treatment of choice for Q fever is tetracycline, doxycycline, or erythromycin. Although not tested, azithromycin and clarithromycin would be expected to be effective.

Prophylaxis

A formalin-inactivated whole cell vaccine is available as an investigational drug in the United States and has been used for those who are at risk of occupational infection with Q fever (Ackland, Worswick, & Marmion, 1994). One dose will provide immunity for an aerosol challenge within 3 weeks.

Skin testing is required to prevent a severe local reac- tion in previously immune individuals. A live attenuated strain (M44) has been used in the former Union of Soviet Socialist Republics (Genig, 1965).

Smallpox Smallpox was used as a BW in the United States during the French and Indian War. Smallpox is an orthopox virus that affects primates, particularly man. The disease was declared eradicated in the world in 1977, and the last reported human case occurred in a laboratory in 1978. Theoretically, the virus exists in only two labo- ratories in the world, one in the United States and one in Russia. The virus can be transmitted by face-to-face contact, droplet nuclei, secretions, and aerosols. It is a durable virus and can exist for long periods outside the host. It is remotely possible that it is still living outside of the repository labs. A very closely related disease, mon- keypox, cannot be easily distinguished from smallpox without significant evaluation of its RNA. A major con- cern of disaster medicine planners is/was the develop- ment of this virus as a war weapon by the former Soviet Union and the unknown amount of product produced at the time.

Release of this virus would have massive and ex- treme societal effects. Although much of world was vac- cinated in the 1960s and 1970s, it is unknown whether those vaccinations would in fact protect an individual. Given that vaccinations were stopped by WHO in 1985, it is supposed that an entire generation could be totally unprotected and thus suffer massive mortality from the disease if it were to be released. Because of the virus’s communicability, only one person need be infected to distribute this virus on an unsuspecting and unprotected world.

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Presentation

Smallpox has a long incubation period of about 10 to 17 days. The illness has a prodrome of 2 to 3 days with malaise, fever, headache, and backache. Over the next 7 to 10 days, all of the characteristic lesions erupt, prog- ress from macules to papules to vesicles to pustules and then crust and scarify (CP FIGURE 9-4). The lesions are more numerous on the extremities and face than on the trunk. The disease is fatal in about 35 percent of cases. Some patients will develop disseminated intravascular coagulopathy. Other complications include smallpox pneumonia, arthritis (a person who had smallpox may have permanent joint deformities), and keratitis (which may cause blindness).

Diagnosis

Like many viral diseases, the diagnosis of smallpox is best made by clinical impression. Routine labs are not helpful, although leukopenia is frequent. Clotting factors may be depressed and thrombocytopenia may be found. Diagnosis may be made with immunofluorescence, elec- tron microscopy, or culture.

Clinical presentation would allow the diagnosis to occur rapidly in most healthcare settings. Much has been written and distributed about smallpox since the failed vaccination program of 2003. As a result, it is likely that any person presenting to most any healthcare clinic or emergency department would be identified rapidly.

Therapy

Therapy for smallpox is entirely supportive. Use of several antiviral medications has been proposed as possible amelioration treatment, but this is untested. It is understood by science that administration of the vaccination post–disease development will likely lessen the disease process and as a rule would be given to all patients, unless they are pregnant or immuno- compromised.

Prophylaxis

Prophylaxis against smallpox has been available since the early 1800s when Dr. Edward Jenner developed a vaccine and is well documented. Because smallpox is presumed to have been eradicated worldwide, there is no recommendation or requirement for routine vacci- nation. Adequate stocks of smallpox vaccine are prob- ably not available for exposure of large portions of the population. It is anticipated that if an outbreak were to occur, institution of a ring vaccination plan (similar to what eradicated the disease) would be immediately instituted, and this would limit the spread.

Objects in contact with a contaminated patient need to be cleansed with live steam or sodium hypochlorite solution.

Tularemia Tularemia or rabbit fever is caused by Francisella tularen- sis, a gram-negative bacillus. Humans can contract this disease by handling an infected animal or by the bites of ticks, mosquitoes, or deerflies. The natural disease has a mortality rate of 5 to 10 percent. As few as 50 organisms can cause disease if inhaled.

Presentation

Like plague, tularemia has an ulceroglandular form, a pneumonic form, and a septicemic form. Two addi- tional forms also occur with tularemia. Oculoglandular tularemia occurs when the inoculum is in the eye. Gastrointestinal tularemia occurs when tularemia bacilli are ingested. It may also infect the oropharynx.

The septicemic form can occur in 5 to 15 percent of natural cases. The clinical features include fever, prostra- tion, and weight loss.

The pneumonic form may occur by inhaling con- taminated dusts or by a deliberate aerosol. The resulting pneumonia is atypical and may be fulminant. Fever, headache, malaise, substernal discomfort, and cough are prominent. The cough is often nonproductive. A chest X-ray may or may not show a pneumonia.

Diagnosis

As noted, the diagnosis of pneumonic tularemia will be difficult clinically, with several types of atypical pneumo- nia as differential diagnoses. The laboratory is unhelpful early in this disease.

Therapy

Human-to-human spread of pneumonic tularemia is unusual and isolation is not required.

Treatment is streptomycin or gentamycin for 10 to 14 days. Tetracycline and chloramphenicol are also useful, but the military reports that there has been a significant relapse rate.

Prophylaxis

A live vaccine strain is available to U.S. military personnel. This vaccine is delivered intradermally and provides pro- tection to an aerosol challenge by the third week postim- munization. Protection is dependent on the inhaled dose of tularemia, and inhalation of massive quantities of bac- teria may overwhelm the protective effects of the vaccine (Hornick & Eigelsbach, 1966). Protection falls after 14 months, suggesting that a booster dose is appropriate. This vaccine is not available for civilian use.

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Chapter Summary

As the emergency service community continues to be subjected to reports of escalating bioterrorism threats, the increase of media attention on the biothreat results in heightened fears and public questions of readiness. Events such as the West Nile virus outbreak immediately result in the press and public fearing that the event was a deliberate act rather than a naturally occurring event.

While the probability of a high-impact or wide- spread attack using BWs is low, the yield from such an event could be devastating. It is for this reason that be- ing prepared to respond to the aftermath of a biological attack is critical. As highlighted in this chapter, there

are many complex issues that nonmilitary responders are not familiar with that accompany the planning and response phases of a bioterrorism event. We strongly recommend that this matter be given the attention it deserves so that your members can be protected and the response effectiveness to your community can be maintained.

Remember that this type of incident can rapidly swell to a level that will overwhelm your EMS system as well as local healthcare resources. Incorporating the talents of your public health and hospital officials in the planning process will provide you with the ability to develop comprehensive and cohesive contingency plans.

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Wrap Up Chapter Questions

1. Define biological warfare. How is a biological at- tack different from other, more traditional forms of terrorism?

2. Briefly discuss the history of biological terrorism. 3. What are the major steps in a biological threat

assessment? 4. What types of PPE are necessary for emergency

responders in a biological event? 5. Discuss the clinical effects, detection, and

prophylaxis/treatment for the following biologi- cal toxins: a. Ricin b. Botulinum toxin c. Clostridium toxin

6. Discuss the clinical effects and treatments for: a. Anthrax

b. Ebola virus c. Tularemia d. Q fever

Chapter Project

Develop a comprehensive outline of a biological threat as- sessment for your jurisdiction or region. Consider key as- sessment elements from this chapter including detection, control of supplies, PPE, training, and prophylaxis.

Vital Vocabulary

Biological terrorism The use of etiological agents (dis- ease) to cause harm or kill a population, food, and/or livestock.

Community shielding An effective and unique pre- paredness strategy to engage individuals, communi- ties, and government in a unified response to disasters and future acts of terrorism, in particular bioterrorism. Originating from the University of Virginia’s Critical Incident Analysis Group, this strategy is being adopted widely as a means of community and organizational resilience.

Enzyme-linked immunosorbent assay An immuno- logical immunoassay technique for accurately measur- ing the amount of a substance, for example, in a blood sample.

Erythrocyte sedimentation rate Also called the sedi- mentation rate or Biernacki reaction, it is the rate at which red blood cells precipitate in a period of one hour; a common hematology test which is a nonspe- cific measure of inflammation. Anticoagulated blood is placed in an upright tube, known as a Westergren tube, and the rate at which the red blood cells fall is measured and reported in mm/h.

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Chapter 7
Chapter 8
Chapter 9

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