ARMY FM 8-284

NAVY NAVMED P-5042

AIR FORCE AFMAN (I) 44-156

MARINE CORPS MCRP 4-11.1C

FIELD MANUAL

TREATMENT OF

BIOLOGICAL WARFARE

AGENT CASUALTIES

HEADQUARTERS, DEPARTMENTS OF THE ARMY, THE NAVY, AND

THE AIR FORCE, AND COMMANDANT, MARINE CORPS

DISTRIBUTION RESTRICTION: Approved for public release; distribution is unlimited.

17 July 2000
C1, FM 8-284

NTRP 4-02.23 (NAVMED P-5042)

AFMAN (I) 44-156

MCRP 4-11.1C

Change 1 HEADQUARTERS

DEPARTMENTS OF THE ARMY,

THE NAVY, AND THE AIR FORCE,

AND COMMANDANT, MARINE CORPS

Washington, DC 8 July 2002

TREATMENT OF BIOLOGICAL WARFARE AGENT CASUALTIES

1. Change FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C, 17 July 2000, as follows:

Remove old pages Insert new pages

i and ii i and ii

1-11 and 1-12 1-11 and 1-12

1-17 and 1-18 1-17 and 1-19

2-1 through 2-4 2-1 through 2-4

2-13 and 2-14 2-13 and 2-14

2-21 and 2-22 2-21 and 2-22

Glossary-3 and Glossary-4 Glossary-3 and Glossary-4

Glossary-7 Glossary-7

References-1 and References-2 References-1 and References-2

Index-3 through Index-6 Index-3 through Index-6

Back cover Back cover

2. New or changed material is indicated by a star ().

3. File this transmittal sheet in front of the publication.

DISTRIBUTION RESTRICTION: Approved for public release, distribution is unlimited.
By Order of the Secretary of the Army:

ERIC K. SHINSEKI

General, United States Army

Official: Chief of Staff

JOEL B. HUDSON

Administrative Assistant to the

Secretary of the Army

By Direction of the Chief of Naval Operations:

Official: R.G. SPRIGG

Rear Admiral, USN

Navy Warfare Development Command

By Order of the Secretary of the Air Force:

Official: PAUL K. CARLTON, JR.

Lieutenant General, USAF, MC, CFS

Surgeon General

By Direction of the Commandant of the Marine Corps:

Official: EDWARD HANLON, JR.

Lieutenant General, U.S. Marine Corps

Commanding General

Marine Corps Combat Development Command

DISTRIBUTION:

US Army: Active Army, USAR, and ARNG: To be distributed in accordance with the initial

distribution number 115795, requirements for FM 8-284.

US Air Force: F

US Marine Corps: PCN: 14400008000

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C
PIN: 077922-000

PCN: 14400008000
i

C1, FM 8-284

NTRP 4-02.23 (NAVMED P-5042)

AFMAN (I) 44-156

MCRP 4-11.1C

FIELD MANUAL HEADQUARTERS

NO. 8-284 DEPARTMENTS OF THE ARMY,

NTRP 4-02.23 (NAVMED P-5042) THE NAVY, AND THE AIR FORCE,

AIR FORCE MANUAL (INTERSERVICE) AND COMMANDANT, MARINE CORPS

NO. 44-156 Washington, DC 17 July 2000

MARINE CORPS

MCRP 4-11.1C

TREATMENT OF BIOLOGICAL WARFARE AGENT CASUALTIES

TABLE OF CONTENTS

Page

PREFACE ......................................................................................... vii

CHAPTER 1. INTRODUCTION

1-1. The Threat of Biological Warfare Agents Against United States

Forces and Civilian Populations ............................................ 1-1

1-2. Modes of Delivery .................................................................. 1-1

1-3. Employment of Biological Warfare Agents .................................... 1-2

1-4. Classification of Biological Warfare Agents ................................... 1-3

1-5. Portals of Entry ..................................................................... 1-3

1-6. Environmental Detection .......................................................... 1-4

1-7. Diagnosis ............................................................................. 1-5

1-8. Specimen Collection ................................................................ 1-6

1-9. Specimen Labeling.................................................................. 1-9

1-10. Specimen Handling and Shipment ............................................... 1-10

1-11. Chain of Custody Responsibilities ............................................... 1-10

1-12. Identification Methods for Biological Warfare Agents ....................... 1-11

1-13. Therapy ............................................................................... 1-12

1-14. Case Reporting and Epidemiological Assessment ............................. 1-12

1-15. Prevention ............................................................................ 1-12

1-16. Protective Equipment............................................................... 1-13

1-17. First Aid .............................................................................. 1-14

1-18. Protective Measures and Handling of Casualties .............................. 1-14

1-19. Patient Decontamination ........................................................... 1-15

1-20. Infection Control .................................................................... 1-16

1-21. Medical Evacuation................................................................. 1-16

1-22. Aeromedical Isolation Team ...................................................... 1-18

 1-23. Investigational New Drugs and Off-Label Indications ........................ 1-18

CHAPTER 2. BACTERIAL AGENTS

Section I. Introduction ......................................................................... 2-1

2-1. General ................................................................................. 2-1

Distribution Restriction: Approved for public release; distribution is unlimited.
ii

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

Page

Section II. Anthrax ................................................................................ 2-1

2-2. General ................................................................................. 2-1

2-3. Biological Warfare Agent Delivery ................................................ 2-2

2-4. Environmental Detection ............................................................ 2-2

2-5. Prevention .............................................................................. 2-2

2-6. Biological Warfare Clinical Presentation ......................................... 2-3

2-7. Diagnosis ............................................................................... 2-3

2-8. Treatment .............................................................................. 2-4

2-9. Control of Patients, Contacts, and Treatment Areas ............................ 2-4

2-10. Medical Evacuation................................................................... 2-4

Section III. Brucellosis ............................................................................. 2-5

2-11. General ................................................................................. 2-5

2-12. Biological Warfare Agent Delivery ................................................ 2-6

2-13. Environmental Detection ............................................................ 2-6

2-14. Prevention .............................................................................. 2-6

2-15. Biological Warfare Clinical Presentation ......................................... 2-7

2-16. Diagnosis ............................................................................... 2-7

2-17. Treatment .............................................................................. 2-7

2-18. Control of Patients, Contacts, and Treatment Areas ............................ 2-8

2-19. Medical Evacuation................................................................... 2-8

Section IV. Melioidosis............................................................................. 2-8

2-20. General ................................................................................. 2-8

2-21. Biological Warfare Agent Delivery ................................................ 2-9

2-22. Environmental Detection ............................................................ 2-9

2-23. Prevention .............................................................................. 2-9

2-24. Biological Warfare Clinical Presentation ......................................... 2-9

2-25. Diagnosis ............................................................................... 2-9

2-26. Treatment .............................................................................. 2-10

2-27. Control of Patients, Contacts, and Treatment Areas ............................ 2-11

2-28. Medical Evacuation................................................................... 2-11

Section V. Glanders ............................................................................... 2-11

2-29. General ................................................................................. 2-11

2-30. Biological Warfare Agent Delivery ................................................ 2-11

2-31. Environmental Detection ............................................................ 2-11

2-32. Prevention .............................................................................. 2-11

2-33. Biological Warfare Clinical Presentation ......................................... 2-12

2-34. Diagnosis ............................................................................... 2-12

2-35. Treatment .............................................................................. 2-12

2-36. Control of Patients, Contacts, and Treatment Areas ............................ 2-13

2-37. Medical Evacuation................................................................... 2-13

Section VI. Plague .................................................................................. 2-13

2-38. General ................................................................................. 2-13

2-39. Biological Warfare Agent Delivery ................................................ 2-14
iii

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Page

2-40. Environmental Detection ............................................................ 2-14

2-41. Prevention .............................................................................. 2-14

2-42. Biological Warfare Clinical Presentation ......................................... 2-14

2-43. Diagnosis ............................................................................... 2-15

2-44. Treatment .............................................................................. 2-15

2-45. Control of Patients, Contacts, and Treatment Areas ............................ 2-16

2-46. Medical Evacuation ................................................................... 2-16

Section VII. Q Fever ................................................................................ 2-16

2-47. General ................................................................................. 2-16

2-48. Biological Warfare Agent Delivery ................................................ 2-17

2-49. Environmental Detection ............................................................ 2-18

2-50. Prevention .............................................................................. 2-18

2-51. Biological Warfare Clinical Presentation ......................................... 2-18

2-52. Diagnosis ............................................................................... 2-19

2-53. Decontamination ...................................................................... 2-19

2-54. Treatment .............................................................................. 2-19

2-55. Control of Patients, Contacts, and Treatment Areas ............................ 2-20

2-56. Medical Evacuation ................................................................... 2-20

Section VIII. Tularemia ............................................................................. 2-20

2-57. General ................................................................................. 2-20

2-58. Biological Warfare Agent Delivery ................................................ 2-21

2-59. Environmental Detection ............................................................ 2-21

2-60. Prevention .............................................................................. 2-21

2-61. Biological Warfare Clinical Presentation ......................................... 2-22

2-62. Diagnosis ............................................................................... 2-22

2-63. Treatment .............................................................................. 2-22

2-64. Control of Patients, Contacts, and Treatment Areas ............................ 2-23

2-65. Medical Evacuation ................................................................... 2-23

CHAPTER 3. VIRAL AGENTS

Section I. Introduction ........................................................................... 3-1

3-1. General ................................................................................. 3-1

Section II. Smallpox ............................................................................... 3-1

3-2. General ................................................................................. 3-1

3-3. Biological Warfare Agent Delivery ................................................ 3-1

3-4. Environmental Detection ............................................................ 3-1

3-5. Prevention .............................................................................. 3-2

3-6. Biological Warfare Clinical Presentation ......................................... 3-3

3-7. Diagnosis ............................................................................... 3-4

3-8. Treatment .............................................................................. 3-4

3-9. Control of Patients, Contacts, and Treatment Areas ............................ 3-4

3-10. Medical Evacuation ................................................................... 3-5
iv

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Page

Section III. Venezuelan Equine Encephalitis ................................................. 3-5

3-11. General ................................................................................. 3-5

3-12. Biological Warfare Agent Delivery ................................................ 3-6

3-13. Environmental Detection ............................................................ 3-6

3-14. Prevention .............................................................................. 3-6

3-15. Biological Warfare Clinical Presentation ......................................... 3-6

3-16. Diagnosis ............................................................................... 3-6

3-17. Treatment .............................................................................. 3-7

3-18. Control of Patients, Contacts, and Treatment Areas ............................ 3-7

3-19. Medical Evacuation ................................................................... 3-7

Section IV. Viral Hemorrhagic Fevers ......................................................... 3-7

3-20. General ................................................................................. 3-7

3-21. Biological Warfare Agent Delivery ................................................ 3-9

3-22. Environmental Detection ............................................................ 3-9

3-23. Prevention .............................................................................. 3-9

3-24. Biological Warfare Clinical Presentation ......................................... 3-9

3-25. Diagnosis ............................................................................... 3-9

3-26. Treatment .............................................................................. 3-10

3-27. Control of Patients, Contacts, and Treatment Areas ............................ 3-10

3-28. Medical Evacuation ................................................................... 3-12

CHAPTER 4. TOXINS

Section I. Introduction ........................................................................... 4-1

4-1. General ................................................................................. 4-1

Section II. Clostridium Botulinum Toxin..................................................... 4-1

4-2. General ................................................................................. 4-1

4-3. Biological Warfare Agent Delivery ................................................ 4-2

4-4. Environmental Detection ............................................................ 4-2

4-5. Biological Warfare Clinical Presentation ......................................... 4-2

4-6. Prevention .............................................................................. 4-3

4-7. Diagnosis ............................................................................... 4-3

4-8. Treatment .............................................................................. 4-3

4-9. Control of Patients, Contacts, and Treatment Areas ............................ 4-5

4-10. Medical Evacuation ................................................................... 4-5

Section III. Clostridium Perfringens Toxins .................................................. 4-5

4-11. General ................................................................................. 4-5

4-12. Biological Warfare Agent Delivery ................................................ 4-5

4-13. Environmental Detection ............................................................ 4-6

4-14. Prevention .............................................................................. 4-6

4-15. Biological Warfare Clinical Presentation ......................................... 4-6

4-16. Diagnosis ............................................................................... 4-6

4-17. Treatment .............................................................................. 4-6
v

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Page

4-18. Control of Patients, Contacts, and Treatment Areas ............................ 4-6

4-19. Medical Evacuation ................................................................... 4-7

Section IV. Ricin .................................................................................... 4-7

4-20. General ................................................................................. 4-7

4-21. Biological Warfare Agent Delivery ................................................ 4-7

4-22. Environmental Detection ............................................................ 4-8

4-23. Prevention .............................................................................. 4-8

4-24. Biological Warfare Clinical Presentation ......................................... 4-8

4-25. Diagnosis ............................................................................... 4-8

4-26. Treatment .............................................................................. 4-8

4-27. Control of Patients, Contacts, and Treatment Areas ............................ 4-9

4-28. Medical Evacuation ................................................................... 4-9

Section V. Saxitoxin ............................................................................... 4-9

4-29. General ................................................................................. 4-9

4-30. Biological Warfare Agent Delivery ................................................ 4-10

4-31. Environmental Detection ............................................................ 4-10

4-32. Prevention .............................................................................. 4-10

4-33. Biological Warfare Clinical Presentation ......................................... 4-10

4-34. Diagnosis ............................................................................... 4-10

4-35. Treatment .............................................................................. 4-11

4-36. Control of Patients, Contacts, and Treatment Areas ............................ 4-11

4-37. Medical Evacuation ................................................................... 4-11

Section VI. Staphylococcal Enterotoxin B..................................................... 4-11

4-38. General ................................................................................. 4-11

4-39. Biological Warfare Agent Delivery ................................................ 4-12

4-40. Environmental Detection ............................................................ 4-12

4-41. Prevention .............................................................................. 4-12

4-42. Biological Warfare Clinical Presentation ......................................... 4-12

4-43. Diagnosis ............................................................................... 4-13

4-44. Treatment .............................................................................. 4-13

4-45. Control of Patients, Contacts, and Treatment Areas ............................ 4-13

4-46. Medical Evacuation ................................................................... 4-13

Section VII. Trichothecene Mycotoxins ......................................................... 4-14

4-47. General ................................................................................. 4-14

4-48. Biological Warfare Agent Delivery ................................................ 4-14

4-49. Environmental Detection ............................................................ 4-14

4-50. Prevention .............................................................................. 4-14

4-51. Biological Warfare Clinical Presentation ......................................... 4-15

4-52. Diagnosis ............................................................................... 4-15

4-53. Treatment .............................................................................. 4-15

4-54. Control of Patients, Contacts, and Treatment Areas ............................ 4-15

4-55. Medical Evacuation ................................................................... 4-15
vi

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Page

APPENDIX A. RECOGNITION OF A BIOLOGICAL WARFARE

AGENT CASUALTY

A-1. General ................................................................................. A-1

A-2. Types of Casualties ................................................................... A-1

A-3. Recognize Biological Casualties .................................................... A-2

APPENDIX B. MEDICAL MANAGEMENT AND TREATMENT IN

BIOLOGICAL WARFARE OPERATIONS

Section I. US Army Medical Treatment Facilities......................................... B-1

B-1. General ................................................................................. B-1

B-2. Objectives of Health Service Support in Biological Warfare Operations.... B-1

B-3. Planning for the Management and Treatment of Biologically

Contaminated Casualties .......................................................... B-2

B-4. Emergency Medical Treatment of Biologically Contaminated

Casualties ............................................................................ B-2

B-5. Patient Decontamination Methods .................................................. B-3

B-6. Logistics ................................................................................ B-5

B-7. Training ................................................................................ B-5

B-8. Casualty Evacuation .................................................................. B-5

Section II. US Air Force Medical Treatment Facilities.................................... B-6

B-9. General ................................................................................. B-6

B-10. Detection of Biological Agents ..................................................... B-7

B-11. Identification ........................................................................... B-8

B-12. Decontamination ...................................................................... B-8

Section III. US Navy Medical Treatment Facilities ......................................... B-9

B-13. General ................................................................................. B-9

GLOSSARY .................................................................................... Glossary-1

Section I. Abbreviations and Acronyms .............................................. Glossary-1

Section II. Definitions ...................................................................... Glossary-6

REFERENCES .................................................................................. References-1

INDEX ........................................................................................ Index-1

PREFACE

Purpose

This publication serves as a guide and a reference for trained members of the Armed Forces Medical

Services and other medically qualified personnel on the recognition and treatment of biological warfare
vii

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

(BW) agent casualties. Information contained in this publication may also be relevant for the diagnosis and

treatment of patients with naturally acquired diseases or illnesses due to pathogens with BW potential.

Scope

a. This publication

(1) Classifies and describes potential BW agents.

(2) Provides procedures for collecting, handling and labeling, shipping, and identifying

potential BW agents.

(3) Describes procedures for medical diagnosing, treating, and management of BW casualties.

(4) Describes medical management and treatment in BW operations.

b. The material in this publication is applicable to both the conventional battlefield and the

integrated environment of the battlefield. (For the purpose of this publication, the integrated environment

is intended to mean warfare and/or contingency operations where nuclear, biological, and chemical [NBC]

weapons/agents are being employed or have a high probability of being employed in addition to conventional

weapons.)

c. The treatment modalities contained in this manual differ from standard textbooks in that they

apply to BW agent exposures. The method of exposure for most BW agents is by inhalation; whereas, the

endemic disease exposure (if applicable) is by other means. Some are by ingestion, some by arthropod

bites, and others by dermal contact with the agent. This does not preclude service members becoming BW

casualties by these means.

d. The use of the term level of care in this publication is synonymous with echelon of care and

role of care. The term echelon of care is the old North Atlantic Treaty Organization (NATO) term.

The term role of care is the new NATO and American, British, Canadian, and Australian (ABCA) term.

Standardization Agreements

This manual is in consonance with the following NATO Standardization Agreements (STANAGs) and

ABCA Quadripartite Standardization Agreements (QSTAGs):

NATO

TITLE STANAG QSTAG

Warning Signs for the Marking of Contaminated or Dangerous Land

Areas, Complete Equipments Supplied and Stores 2002

Reporting Nuclear Detonations, Biological and Chemical Attacks,

and Predicting and Warning of Associated Hazards and Hazard Areas 2103 187

First Aid and Hygiene Training in NBC Operations 2358
viii

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

User Comments

Users of this publication are encouraged to submit recommendations to improve the publication. Comments

should be keyed to the page, paragraph, and line(s) of the text where the change is recommended. The

proponent for this publication is the United States (US) Army Medical Department Center and School

(AMEDDC&S). Comments should be forwarded to: Commander, AMEDDC&S, ATTN: MCCS-FCD,

1400 East Grayson Street, Fort Sam Houston, Texas 78234-6175.

Gender Statement

Unless this publication states otherwise, masculine nouns and pronouns do not refer exclusively to men.

Use of Trade Names/Trademarks

Use of trade names/trademarks in this publication is for illustrative purposes only. Their use does not

constitute endorsement by the Department of Defense (DOD).

References

References listed should be consulted for details beyond the scope of this publication.


	

	
	

	



 	

			
	


	
			


	






























 



	







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C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

• When was the sample/specimen collected?

• Who has maintained custody of the sample/specimen?

• What has been done with the sample/specimen at each change of custody?

CAUTION

Each change of custody must be recorded with date and time of

change.

b. The samples/specimens must be appropriately packaged, labeled, and evacuated to the

designated laboratory for confirmation of a BW attack. The standard chain of custody for sample/specimen

evacuation is as follows:

• Sampling unit.

• Unit S2 (Intelligence Officer [US Army]), medical operations officer, or other designated

person.

• Technical escort unit or other command-designated escort personnel.

• In-theater supporting medical laboratory, if in operation.

• Continental US laboratory.

1-12. Identification Methods for Biological Warfare Agents

The following are identification methods for BW agents:

• Isolation of the etiologic agent by culture (possible in one to two days for some agents).

• Detection of agents by enzyme immunoassay, mass spectrometry, animal inoculation, or other

methods.

• Antibody detection (specific immunoglobulin [IgM] may appear within 3 days).

• Genome detection by PCR.

• Detection of metabolic products of the infectious or toxic agent in clinical specimens.
1-12

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

1-13. Therapy

 a. Endemic Disease versus Biological Agent. Specific therapies are discussed for each agent.

Most of these are based on standard treatment guidelines. However, some of the prophylaxis regimens and

therapies recommended in this manual vary from those found in standard references and may include offlabel indications. This is because—

• A BW exposure (aerosol) may produce a disease with clinical features different from the

naturally occurring disease. For example, inhalation (BW) versus cutaneous (endemic) anthrax. Cases of

endemic disease due to inhalation of some of these agents are rare and clinical experience is limited. Human

challenge studies can be done with only a limited number of agents for obvious ethical and safety reasons.

Accordingly, some of the prophylactic and treatment regimens have been developed from in vitro studies,

animal models, and limited human data.

• An adversary may develop a BW agent resistant to the standard antibiotic therapy.

b. Endemic Disease Therapy. For endemic and epidemic disease therapies, see FM 8-33 and the

civilian textbooks listed in the references.

1-14. Case Reporting and Epidemiological Assessment

It is imperative that clinicians report cases of suspected BW-related illnesses to the appropriate line and

medical chains of command. Prompt epidemiological investigations must begin and preventive measures

implemented to control the disease or reduce the number of cases.

 1-15. Prevention

Most morbidity and mortality from BW threat agents is preventable. Immunizations, pre-exposure chemoprophylaxes, post-exposure chemoprophylaxes, and protective clothing are available to provide protection.

Personnel must have all required immunizations administered prior to entering an AO where BW agent

employment is a threat. All immunizations should be administered in sufficient time to provide the initial

protection before troops are deployed to the AO; when administration prior to deployment is impossible,

troops must receive the immunizations as soon as the mission permits in the AO. Some immunizations are

used in conjunction with pre-exposure chemoprophylaxes or post-exposure chemoprophylaxes to provide

protection. The supporting PHS/PVNTMED units/staffs can assist commanders in determining which

specific immunizations and chemoprophylaxes are required for the AO. The corps/division/wing/equivalent

service/joint task force commander will decide whether to begin, continue, or discontinue the administration

of chemoprophylaxes based on the BW threat. The intelligence officer, chemical officer, and surgeon advise

the commander on appropriate courses of action. For those BW agents that a specific immunization is not

available, the use of protective equipment combined with chemoprophylaxes may be employed to provide

protection.

a. Active Immunization. As of January 1999, vaccines are available for the following potential

BW agent threats:

• Anthrax.

• *Argentine hemorrhagic fever.


	

	
	

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1-17

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

standard precautions as outlined in the Centers for Disease Control and Prevention (CDC) Guidelines for

Isolation Precautions in Hospitals will be followed. If plague, smallpox, and viral hemorrhagic fevers

(VHF) can be reasonably excluded on the basis of analysis of clinical specimens and environmental

samples, patients may be evacuated using Standard Precautions and the disease-specific precautions discussed

for each suspect BW agent in the following chapters.

(3) Biological warfare attacks may occur with multiple agents with short and prolonged

incubation times (botulinum toxin, 12 to 36 hours and smallpox, 7 to 17 days). Multiple agents can lead to

the presence of coinfection-acute illness with short incubation and incubating smallpox (which may declare

itself after patients have been evacuated for evaluation/treatment of the short incubating disease). Therefore,

consideration should be given to quarantining patients for 17 days after AE from the BW area if plague or

smallpox cannot be excluded. Reevaluate patients carefully for recurrent fever or other changes in clinical

status. If clinical or laboratory findings suggest prodromal or syndromic smallpox, plague, or VHFs,

institute appropriate isolation until the diagnosis is clarified. Specific control measures must be applied as

presented for the following diseases/BW agent casualties:

(a) Plague. Plague is an internationally quarantinable disease (IQD). Do not evacuate

across international borders unless authorized by the theater surgeon. Evacuate in cohorts of plague

patients only on dedicated AE aircraft; treat in theater. Pneumonic plague is highly transmissible person-toperson. Droplet precautions are added to standard precautions for patients with pneumonic plague until

sputum cultures are negative.

(b) Smallpox. Currently eradicated and no longer listed as IQD. Immediately notify

the line and medical chain of command upon diagnosis. Do not evacuate across international borders unless

authorized by the theater surgeon. Evacuate in cohorts of smallpox patients only on dedicated AE aircraft;

treat in theater. Smallpox is transmissible person-to-person. Strict quarantine is required. Standard,

contact, and airborne isolation precautions are to be observed. All contacts should be vaccinated and

quarantined/grouped together for at least 17 days following the most recent exposure.

(c) Viral hemorrhagic fevers. The World Health Organization (WHO) does not require

quarantine for hemorrhagic fevers, with the exception of yellow fever. However, due to international

concerns, do not evacuate hemorrhagic fever patients across international borders unless authorized by the

theater surgeon. Evacuate in cohorts of hemorrhagic fever patients only on dedicated AE aircraft. Medical

evacuation may result in increased morbidity and mortality for patients with hemorrhagic fever; treatment at

a local facility is preferred. Person-to-person transmission is possible for the duration of illness. If

necessary, patients may be evacuated using standard, contact, plus respiratory droplet isolation precautions.

(d) Infectious disease of unknown etiology. Evaluate patient evacuation risk based on

the patients’ signs/symptoms complex and theater threat list. Assume infection with the agent requiring the

most stringent infection control procedures (based on the possible threats in the theater and the clinical

picture). Ensure that appropriate patient care is performed while providing the crew and aircraft with the

highest level of protection.

(e) Summary. In summary, many BW agent casualties may be safely evacuated using

basic infection control guidelines. Plague, smallpox, and the hemorrhagic fevers pose significant challenges.
1-18

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

These patient movements will require approval of the destination country, over-flight privileges, and

approval of any country where the aircraft will land for servicing or where patients will remain overnight.

Countries from which approval is sought are bound by Article 37 of the Geneva Conventions for the

Amelioration of the Condition of the Wounded and Sick in Armed Forces in the Field of 12 August 1949 to

ensure humanitarian treatment to wounded and sick. That should include approval under most circumstances

of transit of those injured by exposure to biological agents. Additionally, some countries, notably Germany,

have already developed procedures for expedited approval of transit of dangerous/hazardous goods in their air

space. That information is contained in the DOD Foreign Clearance Guide. Coordination between the theater

or USTRANSCOM commander/surgeon and the Department of State is required for such movements.

1-22. Aeromedical Isolation Team

The USAMRIID maintains an aeromedical isolation team (AIT). The AIT is a rapid response team with

worldwide airlift capability. The AIT is designed to safely evacuate and manage patients with potentially

lethal communicable diseases under high-level containment. Indications for deployment include cases of a

highly contagious, lethal, or unidentified disease, including cases from a suspect BW attack. Diagnosis and

medical care will be provided at USAMRIID. The AIT can only transport a limited number of patients.

The AIT CANNOT provide for mass casualty evacuation. Such evacuation can enhance early identification

of a BW agent; thus, enabling early development of treatment recommendations for medical providers in the

TO. The AIT also offers a portable containment laboratory, limited environmental decontamination, and

specialized consultative expertise.

 1-23. Investigational New Drugs and Off-Label Indications

a. On 30 September 1999, the President of the United States issued Executive Order (EO) 13139,

Improving Health Protection of Military Personnel Participating in Particular Military Operations, which

outlines the conditions under which investigational new drugs (IND) and off-label pharmaceuticals could be

administered to US service members. This publication discusses numerous pharmaceutical products, some

of which are IND. In certain other cases, licensed pharmaceuticals are discussed for use in a manner or for

a condition other than that for which they are licensed (Example: An off-label indication).

b. Executive Order 13139 does not intend to alter the traditional physician-patient relationship or

individual physician prescribing practices. Health care providers remain free to exercise clinical judgment

and prescribe licensed pharmaceutical products as they deem appropriate for the optimal care of their

patients. This policy does, however, potentially influence recommendations that might be made by US

government agencies and that might be applied to large numbers of service members outside of the

individual physician-patient relationship. Key summary points from EO 13139 include:

• The EO describes the Secretary of Defense responsibilities regarding the use of IND

products or off-label use of products as antidotes to chemical, biological, or radiological weapons.

• The EO stipulates that the US Government will administer only FDA-approved products

for their labeled uses. (However, off-label indications and IND usage rules may apply as discussed below

and in other areas of this publication.)
1-19

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

• The EO details IND product use parameters and controls.

• The EO requires individual service member informed consent before IND administration.

However, only the President may waive this informed consent requirement upon request of the Secretary of

Defense if—

• Service member informed consent is not feasible.

• Informed consent is contrary to the best interest of the service member.

• Obtaining informed consent is not in the best interest of national security.
2-1

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

CHAPTER 2

BACTERIAL AGENTS

Section I. INTRODUCTION

2-1. General

Bacterial organisms comprise the greatest number of pathogens in the list of potential BW agents. They

include the etiologic agents of anthrax, brucellosis, cholera, glanders, melioidosis, plague, Q fever, and

tularemia. Of these, anthrax is the most likely BW threat that troops will encounter in an AO. See

Appendix B for guidance on medical management of BW agent casualties.

Section II. ANTHRAX

2-2. General

a. Etiologic Agent. The spores of Bacillus anthracis, an encapsulated gram-positive bacillus.

Sporulation occurs under adverse environmental conditions and when vegetative bacteria are exposed to air;

the spores are extremely hardy and can survive extremes of temperature, dryness, and flooding. When

conditions improve, the spores germinate to produce vegetative bacteria.

b. Reservoir. The soil, with worldwide distribution.

c. Transmission. The stage in the bacterial life cycle, which poses a health hazard, is the spore.

Grazing animals contract spores from the vegetation. Humans contract spores via contact with infected

animals, their hides, wool, or other products; from ingesting contaminated meat; or from inhaling spores

during the processing of wool for textiles. Biting flies in sub-Saharan Africa may also transmit anthrax to

humans. Humans usually do not contract anthrax directly from the soil, unless they work with fertilizers

(bonemeal) prepared from infected animals. Also, humans can contract spores from inhalation of aerosolized

spores released during a BW attack.

d. Endemic Disease. Endemic infectious disease is contracted by inhalation, cutaneous exposure,

oropharyngeal exposure, and ingestion.

(1) Cutaneous anthrax accounts for more than 90 percent of all anthrax cases worldwide.

Disease results when Bacillus anthracis spores are introduced into the skin via inoculation of small cuts/

abrasions or inapparent skin lesions. It may possibly be introduced by biting flies. Cutaneous anthrax

features a painless necrotic ulcer with a black eschar and local edema. The case fatality rate for untreated

cutaneous anthrax is up to 20 percent, but with early, effective therapy is reduced to less than 5 percent.

(2) Oropharyngeal and GI diseases occur following the ingestion of anthrax spores, usually

from consuming meat from infected animals. The clinical features of oropharyngeal and GI anthrax are

discussed below in paragraph 2-6.
2-2

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

(3) Inhalation anthrax occurs when individuals working with animal hides, wool, or bonemeal

inhale the spores. Also, inhalation anthrax may occur from inhalation of aerosolized spores released during

a BW attack. The clinical features of inhalation anthrax are discussed below in paragraph 2-6.

2-3. Biological Warfare Agent Delivery

Aerosolized spores may be delivered by missiles, bomblets, artillery fires, point release, or airborne line

release. Contamination of food and water may also be used.

2-4. Environmental Detection

Nuclear, biological, and chemical teams or other bioenvironmental engineering (BEE) personnel operating

similar detection equipment accomplish detection. Preventive medicine/PHS/BEE personnel perform

detection in water supplies. Detection in food supplies may be performed by veterinary, PVNTMED, or

PHS personnel. Detection in animals may be performed by veterinary personnel.

2-5. Prevention

a. Pre-exposure Prophylaxis. Prevention may be accomplished by immunization plus

chemoprophylaxis.

(1) Immunization. Anthrax vaccine is given in six doses at 0, 2, and 4 weeks and 6, 12, and

18 months, with annual boosting. A minimum of three doses administered within 6 months prior to the

exposure may confer protective immunity.

 (2) Chemoprophylaxis. While the FDA has not approved the use of pre-exposure antibiotics,

empiric evidence indicates their use may significantly reduce morbidity and mortality. Therefore, they

should be considered for use on a case-by-case basis and used as indicated for post-exposure preventive

measures. Such use would require application of IND protocols (see paragraph 1-23).

b. Post-exposure Prophylaxis. Use immunization with chemoprophylaxis to prevent the clinical

manifestation of the disease.

(1) Anthrax vaccine. For personnel who have completed the six-dose series and are up to

date on boosters, or who have received at least three initial doses within 6 months prior to exposure, no

additional doses are indicated, except to complete the series as previously scheduled. For personnel who

have not received any immunizations, begin series and give a minimum of three doses; complete the sixdose series, if possible. Use of anthrax vaccine post-exposure requires application of an IND protocol.

 (2) Chemoprophylaxis. Chemoprophylaxis is recommended as an adjunct to immunization

for post-exposure prophylaxis. All personnel exposed to aerosolized anthrax should be administered

Ciprofloxacin hydrochloride tablets (500 mg) orally every 12 hours for 60 days. When Ciprofloxacin
2-3

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

hydrochloride tablets are not available, doxycycline hyclate tablets (100 mg) should be taken orally every

12 hours for 60 days. The duration of chemoprophylaxis administration for individuals without receipt of

any vaccine should be extended until they receive at least three doses of vaccine. Chemoprophylaxis should

be withdrawn under careful observation and with access to an MTF with intensive care and consultative

assets. If fever develops following the withdrawal of chemoprophylaxis, empiric therapy for anthrax is

indicated pending etiologic diagnosis.

2-6. Biological Warfare Clinical Presentation

a. Incubation Period. The incubation for anthrax is hours to 7 days. Most cases present within

48 hours post-exposure.

b. Signs and Symptoms.

(1) Inhalation anthrax. Inhalation anthrax will begin with nonspecific symptoms of fever,

malaise, and fatigue. A nonproductive cough and vague chest discomfort may be present. These initial

symptoms may be followed by a short period of symptomatic improvement, hours to 3 days in duration.

This will be followed by an acute phase, including the abrupt onset of severe respiratory distress with

dyspnea, stridor, diaphoresis, and cyanosis. Bacteremia and toxemia, septic shock, metastatic infection

(meningitis in approximately 50 percent of the cases), and death usually occurs within 24 to 36 hours from

the onset of the acute phase.

(2) Oropharyngeal or gastrointestinal anthrax. Oropharyngeal or GI anthrax can occur

following ingestion of food contaminated with anthrax spores.

(a) Oropharyngeal anthrax will present with initial symptoms of fever, sore throat, and

difficulty swallowing. The disease may progress to an acute phase with symptoms including a necrotic

ulcer or eschar involving the hard palate, tonsils, or posterior oropharyngeal wall, edema of cervical tissues

(possibly resulting in upper airway obstruction), and cervical lymphadenopathy. Most acute cases progress

to septic shock and death.

(b) Gastrointestinal anthrax begins with vague initial symptoms featuring fever, anorexia,

nausea, and vomiting. Abdominal pain, bloody vomiting, bloody diarrhea, and possibly massive abdominal

swelling (ascites) may follow these symptoms. Also, septic shock and death may follow these symptoms.

2-7. Diagnosis

During the incubation period, nasal swabs and specimens of respiratory secretions sent for PCR are the

most important diagnostic specimens. During the early disease, blood and respiratory secretions may be

sent for rapid identification by genetic typing (PCR). A rapid diagnostic test is available that detects toxin

antigens in the blood during the acute phase. Chest x-ray may be normal or show hilar adenopathy early in

the illness and may show a widened mediastinum and pleural effusions during the acute phase.
2-4

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

2-8. Treatment

a. Triage Categories. Patients presenting with initial signs of inhalation anthrax should be placed

in the Immediate category, as early aggressive treatment is lifesaving. Depending on the numbers of cases

and available resources, patients presenting in the acute phase of inhalation anthrax should be placed in the

Immediate or Expectant categories.

b. Medical Management.

(1) Supportive care includes maintaining the airway, providing resuscitative fluids, and

providing vasopressors as indicated for shock.

(2) Specific therapy includes the administration of ciprofloxacin (400 mg intravenous [IV]

every 12 hours) or doxycycline (200 mg IV loading dose, followed by 100 mg IV every 12 hours). Specific

therapy may also include administration of penicillin (4 million units IV) every 4 hours, if isolate is sensitive

to penicillin.

(3) A tracheostomy is indicated for upper airway obstruction due to oropharyngeal anthrax.

Surgical debridement of cutaneous lesions is contraindicated. Surgical drainage of the mediastinum for

inhalation anthrax is not recommended.

c. Prognosis. The number of cases of inhalation anthrax occurring during the antibiotic era is

too small to establish case fatality rates and efficacy of treatment. Almost all inhalation anthrax cases in

which treatment was begun after onset of significantly severe symptoms have been fatal, regardless of

treatment. Despite medical therapy, most patients with inhalation anthrax die within 24 hours of the onset

of the acute phase of the illness. However, in nonhuman primate trials, animals have responded to aggressive

therapy. The prognosis for oropharyngeal and GI anthrax is poor, with case fatality rates 50 to 100 percent,

even with aggressive therapy.

2-9. Control of Patients, Contacts, and Treatment Areas

• Report all cases to line and medical chains of command.

• Employ Standard Precautions for handling, treating, and moving all active cases.

• Use sporicidal agents, such as disinfectant strength iodophors, in MTFs for general area

disinfection. Antiseptic strength iodophors are not sporicidal. Hypochlorite solutions may be attenuated by

organic matter, but will provide a disinfectant capability when used in a 5-percent solution. The hypochlorite

solution should be replaced frequently. Autoclaving, steam sterilizing, or burning is required for complete

eradication of spores.

2-10. Medical Evacuation

Patients with anthrax may be evacuated with other categories of patients. Anthrax is not transmissible

person to person. Standard Precautions should be observed during evacuation.
2-5

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Section III. BRUCELLOSIS

2-11. General

a. Etiologic Agent. The genus Brucella is encapsulated nonmotile bacteria consisting of short,

gram-negative coccoid bacillus. There are four members of the genus Brucella that are human pathogens.

These are Brucella melitensis, Brucella abortus, Brucella suis, and Brucella canis.

b. Reservoir. The following are reservoirs in nature for the disease:

 Brucella melitensis. Primarily sheep, goats, and camels. It may also be found in bison,

elk, caribou, and some species of deer.

 Brucella abortus. Cattle.

 Brucella suis. Swine.

 Brucella canis. Dogs and coyotes.

The organisms may be produced in a laboratory for BW purposes, using a single cell or a small amount of

the organism from a natural source.

c. Transmission. The disease is transmitted to humans by

 Inhalation of aerosols or dusts that contain organisms.

 Ingestion of unpasteurized dairy products and contaminated meat.

 Inoculation of abraded skin or mucosal surfaces.

d. Endemic Disease.

(1) Pathogenesis. Following introduction into the body, Brucella organisms are phagocytized

by polymorphonuclear or mononuclear cells and are transported to regional lymph nodes. However,

Brucella organisms can survive intracellularly. This results in the release of bacteria from lysed cells,

resulting in hematogenous metastasis to other organs, particularly organs high in reticuloendothelial content

(notably the liver, spleen, bone marrow, and possibly, the lungs).

(2) Acute disease. Onset may be sudden or insidious (in approximately one half of all cases)

with nonspecific symptoms of fever, malaise, fatigue, anorexia, weight loss, and depression. Illness

persists as a systemic illness, with or without localizing signs and symptoms. Fever can be intermittent.

Physical examinations may be unrevealing or may disclose fever, mild lymphadenopathy, and

hepatosplenomegaly. Disease localization can occur, usually in tissues high in reticuloendothelial content.
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(3) Osteoarticular. Bone and joint disease is the most common localizing complications,

occurring in up to 40 percent of cases. These include bursitis, sacroiliitis, spondylitis, peripheral joint

arthritis, and osteomyelitis. Vertebral osteomyelitis can result in epidural abscess resulting in spinal cord

compression, and psoas abscess. In addition to developing pyogenic septic osteoarticular infection, patients

may also develop reactive arthropathies. Diagnostic studies can include magnetic resonance imaging (MRI),

computed tomography (CT), and technetium bone scans; plain radiographs may be insensitive early in disease.

(4) Pulmonary infection. Although the respiratory tract is a portal of entry for brucellosis,

pulmonary disease is rare, under 15 percent. Complications may include hilar and paratracheal adenopathy,

interstitial pneumonia, pulmonary nodules, pleural effusions, and empyema.

(5) Genitourinary tract infection. Acute orchitis or epididymo-orchitis are the most common

genitourinary (GU) complications, usually in the absence of systemic symptoms or signs. Intrapartum

infection is rare, but can result in abortion although there is no convincing evidence that the risk is higher

than that of other bacteremic infections. Early diagnosis and therapy will prevent an adverse outcome.

Chronic pyelonephritis has been reported as a rare complication.

(6) Cardiovascular. Endocarditis occurs in less than 2 percent of the cases, but accounts for

most deaths from brucellosis. Other cardiovascular complications may include pericarditis, myocarditis,

and mycotic aneurysms.

(7) Neurologic. Acute or chronic meningitis occurs in less than 2 percent of the cases.

Depression, fatigue, and headache occurring in most cases represent nonspecific features of systemic disease.

2-12. Biological Warfare Agent Delivery

The primary threat is by aerosol release. A foodborne brucellosis attack is unlikely, but could be executed.

2-13. Environmental Detection

Currently, detection is primarily by laboratory analysis of specimens from patients presenting with the

illness or by laboratory testing of foods for the organism. Veterinary/PVNTMED/ PHS/BEE personnel

should collect samples from dairy products and other food items suspected of being contaminated with the

organism. Field NBC reconnaissance teams may collect the agent from an aerosol cloud, but must rely on

the supporting medical laboratory for identification.

2-14. Prevention

a. Pre-exposure Prophylaxis. Vaccines are not currently available for human use; attenuated vaccines

for veterinary use have caused brucellosis following accidental percutaneous or mucous membrane exposures.

Chemoprophylaxis has not been proven to be effective and may delay or mask the onset of the disease.
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b. Post-exposure Prophylaxis. A 3- to 6-week course of therapy is advised following high-risk

exposures to attenuated vaccines for veterinary use, which have been associated with human disease.

Accordingly, a full course of therapy (see paragraph 2-17) is advised for exposed personnel following a

proven brucellosis BW attack. Post-exposure chemoprophylaxis is generally not advised following possible

natural exposures to endemic disease. Personnel must avoid consuming unpasteurized dairy products or

uncooked foods containing the dairy products and avoid contact with suspect infected animals.

2-15. Biological Warfare Clinical Presentation

a. Incubation. Incubation varies from 5 days to 8 weeks, usually 2 to 8 weeks.

b. Signs and Symptoms. See endemic disease above.

2-16. Diagnosis

A definitive diagnosis is made by culturing the organism from blood, bone marrow, or other clinical

specimens. The laboratory should be advised to maintain cultures for at least 4 weeks, as Brucella species

grow slowly in vitro. The sensitivity of cultures varies with clinical specimens; 15 to 70 percent for blood,

greater than 90 percent for bone marrow. Isolates may be misidentified as Moraxella or Haemophilus

species in automated bacterial identification systems that lack specific profiles for Brucella species. Submit

specimens for ELISA testing and PCR. Serologic tests are valuable for diagnosis. Most patients with

brucellosis will have serum-agglutinating titers (SAT) of 1:160 or greater; lower titers must be analyzed

within the patients clinical context. The SAT will not detect antibodies to Brucella canis; a specific test is

required. False negative tests may occur because of blocking antibodies; dilution to 1:320 or a Coombs

test is indicated for suspected cases with negative titers.

2-17. Treatment

a. Triage Categories. Triage categories will vary with conditions and available resources.

Given the subacute nature of brucellosis, most patients are candidates for the Delayed treatment category.

b. Medical Management.

(1) Undifferentiated febrile illness. Antibiotic therapy requires a combination of two

medications. Administer

 Doxycycline, 200 mg, daily for 6 weeks and rifampin, 600 mg, daily for 6 weeks or

 Doxycycline, 200 mg, daily for 6 weeks and streptomycin, 1 gm intramuscularly

(IM), daily for 2 weeks.

(2) Osteoarticular disease. Treat as indicated in (1) above, but extend therapy to 12 weeks.
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(3) Endocarditis. Administer antibiotic therapy as indicated in (1) above. Optimal duration

of therapy is undefined; however, treatment is often continued for 6 to 9 months. Surgical heart valve

replacement is usually necessary for total cure and should be strongly considered.

(4) Central nervous system (CNS) disease. Administer antibiotic therapy as indicated in (1)

above, but extend therapy for 6 to 9 months.

(5) Abscesses. In addition to treatment in (1) above, drainage of abscesses should be done as

surgically indicated.

c. Prognosis. The case fatality rate for untreated brucellosis has historically been less than 2

percent. Most fatalities in untreated cases result from endocarditis due to Brucella melitensis. Untreated

brucellosis may result in severe morbidity for months, and occasionally years.

2-18. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions for disease control. The disease is not communicable from person to person.

2-19. Medical Evacuation

Patients with brucellosis are evacuated with other patients. Apply Standard Precautions for disease control.

Section IV. MELIOIDOSIS

2-20. General

a. Etiologic Agent. Burkholderia (B.) pseudomallei (formerly Pseudomonas pseudomallei), a

small, gram-negative aerobic bacillus.

b. Reservoir. Soil and water throughout the world between 20 degrees north and south latitudes.

Several animals, including sheep, goats, horses, swine, monkeys, and rodents, serve as reservoirs.

However, there is no evidence that animals are important reservoirs, except that they spread the agent to

new foci (soil and water).

c. Transmission. Inoculation of gross or inapparent skin lesions from contact with contaminated

soil or water, aspiration or ingestion of contaminated water, or inhalation of contaminated dust.

d. Endemic Disease. Acute pulmonary disease is the most common form of the endemic disease.

Acute local suppurative disease can complicate inoculation of the skin, resulting in a nodular lesion at the

portal of entry, with lymphangitis and regional lymphadenopathy. Acute septicemic disease and chronic

suppurative sequelae are discussed in paragraph 2-24.
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2-21. Biological Warfare Agent Delivery

The primary threat is aerosol release.

2-22. Environmental Detection

The NBC reconnaissance team collects samples from aerosol clouds; PVNTMED/PHS/BEE personnel

collect samples from soil and water sources; and veterinary/PVNTMED/PHS personnel collect samples

from food supplies/sources. The supporting medical laboratory processes the samples and provides the

command with initial identification of the organism.

2-23. Prevention

Currently, no pre-exposure or post-exposure prophylaxis is available.

2-24. Biological Warfare Clinical Presentation

a. Incubation. 10 to 14 days following inhalation.

b. Signs and Symptoms.

(1) Following an aerosol attack, melioidosis will most likely present as an acute pulmonary

infection. Infection can vary from a mild bronchitis to a severe necrotizing pneumonia. The illness may

begin abruptly, or with a vague prodrome featuring headache, anorexia, and myalgia. Fever, often in

excess of 102° Fahrenheit (F), is common. Localizing symptoms may include pleuritic or dull aching chest

pain, and a cough (which may be either productive or nonproductive of purulent or bloody sputum).

Physical findings may be minimal but can feature pulmonary rales. Acute pulmonary disease can progress

and result in bacteremia and acute septicemic disease.

(2) The acute septicemic disease may follow a terminal course with death occurring in 7 to

10 days. Case fatality rate for acute septicemic disease exceeds 90 percent. Symptoms may include severe

dyspnea, headache, pharyngitis, diarrhea, and a pustular rash. Physical findings may include high fever,

tachypnea, hypotension, flushing of the skin, cyanosis, and rash (the rash may begin as a generalized

papular rash that may progress to a pustular exanthem). Chest findings are variable; palpable

hepatosplenomegaly may be present.

(3) Pulmonary infection can result in chronic disease, with clinical and radiographic features

similar to those of tuberculosis. Chronic suppurative disease can complicate metastatic infection to other

organs including the brain, myocardium, liver, bone, spleen, lymph nodes, and eyes.

2-25. Diagnosis

Microscopic evaluation of exudate will feature poorly staining gram-negative bacilli; methylene blue or

Wrights stain will disclose a safety pin bipolar appearance. Standard bacteriologic culture methods can
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identify B. pseudomallei. Diagnosis can also be confirmed by serologic tests, with the limitations that single

low titers are nondiagnostic and negative serology does not exclude the diagnosis. Given the possible

presentation of an acute pneumonia and the above findings on sputum studies, the most important item in a

differential diagnosis, especially in a BW context, would be plague (see paragraph 2-38). Chest x-rays may

disclose infiltrates involving the upper lobes, with consolidation and cavitation. Pleural effusions and

pleural-based masses are unusual radiographic findings. Leukocyte count can vary from normal to 20,000

white blood cells/cubic millimeter.

2-26. Treatment

a. Triage Categories. Triage categories will vary based upon the stage and severity of illness and

available resources. Patients with signs and symptoms of acute pulmonary disease are classified as Immediate

or Delayed category, depending on severity of presentation. Those presenting in septic shock are classified

as Immediate or Expectant category, depending on available resources.

b. Medical Management. In medical management, therapy will vary with the type and severity

of the clinical presentation.

(1) For localized disease, administer one of the following for a duration of 60 to 150 days:

 Amoxicillin/clavulanate, 60 mg/kilograms (kg)/day in 3 divided oral doses.

 Tetracycline, 40 mg/kg/day in 3 divided oral doses.

 Trimethoprim/sulfa (TMP, 4 mg per kg per day/sulfa, 20 mg per kg per day in

divided oral doses).

(2) For localized disease with mild toxicity, administer antibiotics as follows: Combine two

of the above oral regimens for a duration of 30 days, followed by monotherapy with either amoxicillin/

clavulanate or TMP/sulfa for 60 to 150 days. For extrapulmonary suppurative disease, the antibiotic

therapy should be administered for 6 to 12 months. Surgical drainage of abscesses is indicated.

(3) For severe and/or septicemic disease, administer antibiotics as follows: Ceftazidime,

120 mg/kg/day in three divided doses, combined with TMP/sulfa (TMP, 8 mg per kg per day/sulfa, 40 mg

per kg per day in four divided doses). Initially, administer parenteral therapy for 2 weeks, followed by oral

therapy for 6 months.

(4) The addition of streptomycin is indicated if presentation (acute pneumonia) and sputum

studies suggests plague (see paragraph 2-38).

c. Prognosis. The extent of infection will vary with inoculum, individuals underlying state of

health, availability of protective mask or other respiratory protective devices, and other factors. Late

activation or recrudescence can result years or decades later.
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2-27. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in management of patients and contacts. Melioidosis, glanders, and smallpox

may present with diffuse pustular rashes; strict isolation and quarantine would be indicated until smallpox

can be excluded. Contact precautions are indicated while caring for patients with skin involvement.

Melioidosis, glanders, and smallpox may present as acute pulmonary disease with purulent sputum.

Respiratory isolation pending exclusion of plague is prudent if sputum studies disclose gram-negative bacilli

with bipolar safety pin when using Wrights or methylene blue stains.

2-28. Medical Evacuation

Patients may be evacuated following the exclusion of smallpox and plague. Contact precautions are

indicated for patients with skin involvement.

Section V. GLANDERS

2-29. General

a. Etiologic Agent. B. mallei (formerly Pseudomonas mallei), is a gram-negative bacillus.

b. Reservoir. Horses, mules, and donkeys serve as reservoirs.

c. Transmission. By the organism invading the nasal, oral, and conjunctival mucous membranes,

by inhalation into the lungs, and by invading abraded or lacerated skin. Inhalation of aerosols from cultures

by laboratory workers has occurred.

d. Endemic Disease. The disease is not widespread. The cases have been among veterinarians,

horse and donkey caretakers, abattoir workers, and laboratory personnel.

2-30. Biological Warfare Agent Delivery

The primary threat is aerosol release.

2-31. Environmental Detection

The NBC reconnaissance team collects samples from aerosol clouds; veterinary personnel collects specimens

from animals.

2-32. Prevention

Currently, no pre-exposure or post-exposure prophylaxis is available.
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2-33. Biological Warfare Clinical Presentation

a. Incubation Period. 10 to 14 days after inhalation.

b. Signs and Symptoms. Fever, rigors, sweating, myalgia, headache, pleuritis, chest pain,

cervical adenopathy, splenomegaly, and generalized papular/pustular eruptions.

2-34. Diagnosis

Methylene blue stain of exudates may reveal scant small bacilli. Chest x-ray may show miliary lesions,

small multiple lung abscesses, or bronchopneumonia. B. mallei can be cultured from infected secretions

using meat nutrients.

2-35. Treatment

a. Triage Categories. Triage categories will vary based upon the stage and severity of illness and

available resources. Patients with signs and symptoms of acute pulmonary disease are classified as Immediate

or Delayed category, depending on severity of presentation. Those presenting in septic shock are classified

as Immediate or Expectant category, depending on available resources.

b. Medical Management. In medical management, therapy will vary with the type and severity

of the clinical presentation.

(1) For localized disease, administer one of the following for a duration of 60 to 150 days:

 Amoxicillin/clavulanate, 60 mg/kg/day in 3 divided oral doses.

 Tetracycline, 40 mg/kg/day in 3 divided oral doses.

 Trimethoprim/sulfa (TMP, 4 mg per kg per day/sulfa, 20 mg per kg per day in

divided oral doses).

(2) For localized disease with mild toxicity, administer antibiotics as follows: Combine two

of the above oral regimens for a duration of 30 days, followed by monotherapy with either amoxicillin/

clavulanate or TMP/sulfa for 60 to 150 days.

(3) For extrapulmonary suppurative disease, the antibiotic therapy should be administered

for 6 to 12 months. Surgical drainage of abscesses is indicated.

(4) For severe and/or septicemic disease, administer antibiotics as follows: Ceftazidime,

120 mg/kg/day in three divided doses, combined with TMP/sulfa (TMP, 8 mg per kg per day/sulfa, 40 mg

per kg per day in four divided doses). Initially, administer parenteral therapy for 2 weeks, followed by oral

therapy for 6 months.
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(5) The addition of streptomycin is indicated if presentation (acute pneumonia) and sputum

studies suggests plague.

c. Prognosis. The extent of infection will vary with inoculum, individual’s underlying state of

health, availability of protective mask or other respiratory protective devices, and other factors. Late

activation or recrudescence can result years or decades later.

2-36. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in management of patients and contacts. Glanders, melioidosis, and smallpox

may present with diffuse pustular rashes; strict isolation and quarantine would be indicated until smallpox

can be excluded. Contact precautions are indicated while caring for patients with skin involvement.

Glanders, melioidosis, and smallpox may present as acute pulmonary disease with purulent sputum.

Respiratory isolation pending exclusion of plague is prudent if sputum studies disclose gram-negative bacilli

with bipolar “safety pin” appearance when using Wright’s or methylene blue stains.

2-37. Medical Evacuation

Patients may be evacuated using Standard Precautions following the exclusion of plague.

Section VI. PLAGUE

2-38. General

a. Etiologic Agent. Yersinia pestis (Y. pestis) is a gram-negative bacillus of the family

Enterobacteriaceae.

b. Reservoir. The primary reservoir is rodents. Domestic cats and wild carnivores can also

transmit plague to humans.

c. Transmission. In endemic or epidemic plague, the disease is transmitted via infected fleas

from rodent to human, dog or cat to human, or person to person. Respiratory droplet transmission can

occur person to person or cat to person. Respiratory transmission is enhanced in humid climates. Plague

may also be transmitted via cat bites or scratches.

d. Endemic Disease.

(1) Bubonic plague features the acute onset of fever and prostration in association with

acute, painful lymphadenitis in the lymph node group draining the site of the fleabite. A skin lesion at the

portal of entry (site of fleabite) is seen in less than 25 percent of cases; clinically apparent lymphangitis does

not occur. The disease progresses with bacteremia, resulting in metastatic infection, septic shock, and
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thrombosis of small arteries, resulting in digital gangrene. Pneumonia due to hematogenous metastasis

occurs in approximately 25 percent of cases. The case fatality rate for untreated bubonic plague is

approximately 60 percent, but is less than 5 percent with prompt, effective therapy.

(2) Primary pneumonic plague occurs after inhalation of organisms, which may occur via

aerosol transmission from a person or animal with secondary or primary pneumonic plague.

(3) Septicemic plague may evolve from any form of plague. It features the acute onset of

bacteremia, septic shock, and thrombosis with or without antecedent lymphadenitis. Prognosis for

pneumonic and septicemic pneumonic plague is poor; the fatality rate is 100 percent for untreated cases.

2-39. Biological Warfare Agent Delivery

The primary threat is by aerosol release or by contamination of food and water.

2-40. Environmental Detection

The NBC reconnaissance teams may collect the agent from an aerosol cloud. Preventive medicine/PHS/

BEE personnel may collect suspect soil or water samples. Veterinary/PVNTMED/PHS personnel may collect

samples from suspect contaminated food. A plague BW attack may result in simultaneous onset of disease in

humans, rodent reservoirs, and possibly domestic and wild animals not usually associated with plague.

2-41. Prevention

a. Repellents. Use of insect repellents, approved for human use, will provide a level of protection

from bites by infected fleas.

b. Immunization. The currently available inactivated whole cell vaccine is not recommended for

protection from the BW agent; it does not protect laboratory animals from aerosolized plague. However,

the vaccine is effective in preventing bubonic plague among troops deployed in endemic/epidemic areas (see

endemic disease, above).

 c. Pre-exposure Prophylaxis. While the FDA has not approved the use of pre-exposure

antibiotics, empiric evidence indicates their use may significantly reduce morbidity and mortality. Therefore,

they should be considered for use on a case-by-case basis and used as indicated for post-exposure preventive

measures. Such use would require application of IND protocols (see paragraph 1-23).

d. Post-exposure Prophylaxis. Administer doxycycline 100 mg orally every 12 hours for one

week or ciprofloxacin 500 mg orally every 12 hours for one week.

2-42. Biological Warfare Clinical Presentation

a. Incubation. 2 to 10 days.
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b. Signs and Symptoms. Following an aerosol release of the organisms, unprotected individuals

will present with acute pneumonic plague featuring high fever, systemic toxicity, productive cough, and

hemoptysis. Chest x-ray findings are discussed in paragraph 2-43. Patients may present with disseminated

intravascular coagulation (DIC) with resultant thrombosis and digital gangrene. However, hemorrhagic

complications of DIC in plague are rare. Further, an aerosol attack of plague could result in an epidemic of

bubonic plague if rodent hosts and flea vectors are present in the vicinity of the attack.

2-43. Diagnosis

Gram stain of expectorated sputum may disclose gram-negative bacilli; Giemsa or Van Wayson stains may

disclose blue-staining bacilli with a bipolar safety pin appearance. Organisms may be visualized on

peripheral blood smears during bacteremia. Cultures of blood and respiratory secretions are indicated.

Findings on a chest x-ray may include patchy peribronchial infiltrates, cavitation, consolidation, hilar

adenopathy, and pleural effusions. Other findings may include leukocytosis (at times severe leukemoid

reaction) and abnormal coagulation studies consistent with DIC. Differential diagnosis should include other

causes of acute pneumonia.

2-44. Treatment

a. Triage Categories. The triage category varies with conditions and available resources. Plague

pneumonia is curable if treatment is begun early; therefore, these patients are classified as Immediate.

Patients presenting after 24 hours following the onset of respiratory symptoms are less likely to survive;

they are classified as Expectant.

b. Medical Management.

(1) Supportive care. Supportive care should include IV hydration, supplemental oxygen,

and respiratory support as indicated.

(2) Specific therapy. Administer one of the following:

 Streptomycin, 15 mg/kg lean body mass IM every 12 hours for 10 to 14 days.

 Gentamicin, 5 mg/kg lean body mass IV every 24 hours for 10 to 14 days.

 Gentamicin, 1.75 mg/kg lean body mass IV every 8 hours for 10 to 14 days.

 Ciprofloxacin, 400 mg IV every 12 hours. Oral therapy may be given (750 mg orally

every 12 hours) after the patient is clinically improved, for completion of a 10- to 14-day course of therapy.

 Doxycycline, 200 mg IV loading dose followed by 100 mg IV every 12 hours. Oral

therapy may be given (100 mg orally every 12 hours) after the patient is clinically improved, for completion

of a 10- to 14-day course of therapy.
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(3) Plague meningitis. Administer chloramphenicol 25 mg/kg IV loading dose, followed by

15 mg/kg IV every 6 hours. Oral therapy may be given after the patient is clinically improved, for

completion of a 10- to 14-day course of therapy.

c. Prognosis. Pneumonic plague is invariably fatal if antibiotic therapy is delayed more than 1

day after the onset of symptoms.

2-45. Control of Patients, Contacts, and Treatment Areas

Pneumonic plague is a very contagious disease; control of patients, contacts, and treatment areas is critical

in preventing spread of the disease. The following must be applied for all cases:

 Report case(s) to line and medical chains of command.

 Employ Standard Precautions for disease control. For suspected pneumonic plague (BW

presentation), apply respiratory droplet isolation for a minimum of the first 48 hours of therapy. If plague

pneumonia is confirmed, continue respiratory droplet isolation until sputum cultures are negative.

 Employ measures to minimize personnel contact with rodents (proper food storage, trash

disposal, and elimination of rodent nests); enforce the use of topical insect repellents and the use of

insecticides in and around troop encampments to kill fleas, thus decreasing the risk of secondary

transmission. Eliminate fleas from patients and their personal effects.

 Administer post-exposure prophylaxis to immediate contacts as described paragraph 2-41 above.

 Conduct terminal disinfection of all items used in the care of patients. The standard

disinfectants available at MTFs will inactivate Y. pestis.

2-46. Medical Evacuation

Quarantine patients. Evacuate only with other plague cases. Employ respiratory droplet precautions in

addition to Standard Precautions for patients with pneumonic plague until sputum cultures are negative. Do

not evacuate across international borders unless authorized by senior medical leadership (see paragraph

1-21 for additional information).

Section VII. Q FEVER

2-47. General

a. Etiologic Agent. Coxiella (C.) burnetii is a rickettsial organism that is highly resistant to heat

and desiccation. The organism is highly communicable via aerosol. A single viable organism is enough to

cause infection in humans.
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b. Reservoir. The reservoir is sheep, goats, cattle, dogs, cats, some wild mammals, birds, and

ticks. Infected animals usually do not develop the disease, but shed large numbers of organisms (109

organisms per gram) in placental tissues and body fluids.

c. Transmission. The organisms are usually transmitted via aerosols containing dust from areas

contaminated by placentas, amniotic fluid, excreta from infected animals, aerosols generated by processing

products of infected animals, direct contact with infected animals, and/or ingestion of unpasturized milk.

Q fever has also been transmitted by inhaling aerosols generated from manure, straw, contaminated laundry,

and vehicles. The role of ticks as vectors of human disease is unclear, but they may transmit the disease to

humans by dropping organisms on the body at the site of their bite.

d. Endemic Disease. Acute Q fever can present as an undifferentiated febrile illness, as an

atypical pneumonia, or as a rapidly progressive pneumonia.

(1) The atypical pneumonia presentation features fever, fatigue, chills, sweats, and

myalgia. Approximately 75 percent of patients will complain of severe headache. There is a relative

absence of respiratory symptoms; coughing occurs in approximately 25 percent of patients with radiography

confirmed pneumonia. Physical examination of the chest is usually normal; inspiratory rales may be

present. Patients with the rapidly progressive pneumonic presentation may feature auscultatory findings

consistent with consolidation. Q fever pneumonia can result in development of hyponatremia due to the

syndrome of inappropriate antidiuretic hormone (SIADH).

(2) Neurologic complications of Q fever include aseptic meningitis or encephalitis in

approximately 1 percent of cases. Other complications have included cranial nerve palsies, behavioral

disturbances, cerebellar and extrapyramidal disease, and Miller Fisher syndrome. Other rare extrapulmonary

complications have included hemolytic anemia and glomerulonephritis.

(3) Approximately 33 percent of Q fever cases will develop acute hepatitis (Q fever hepatitis).

The acute hepatitis can present with fever and abnormal liver function tests with the absence of pulmonary

symptoms, signs, or radiographic abnormalities. A liver biopsy may disclose granulomatous hepatitis with

a highly suggestive histologic appearance. The granuloma will present as a dense fibrin ring surrounded by

a central lipid vacuole (doughnut granuloma).

(4) Endocarditis is usually a manifestation of chronic Q fever. Patients with valvulopathies

or other anatomic abnormalities of the vascular tree are at increased risk. Routine blood cultures will be

negative. Fever may be absent. Typical findings include clubbing of the fingernails, hepatosplenomegaly

in approximately 50 percent of cases, arterial embolic phenomena in 33 percent of cases, and purpura due

to leukocytoclastic vasculitis in approximately 20 percent of cases.

2-48. Biological Warfare Agent Delivery

The primary threat is by aerosol or through contamination of food.
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2-49. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory analysis and confirmation.

Medical personnel collect medical specimens for supporting laboratory analysis and confirmation.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples for supporting laboratory

analysis and confirmation.

2-50. Prevention

a. Miscellaneous. The military protective mask provides protection from aerosols. Only consume

pasteurized dairy products and heat all foods sufficiently to destroy the organisms.

b. Pre-exposure Prophylaxis. A formalin-inactivated whole cell vaccine is available under IND

status. A single dose of vaccine provides protection for at least five years. The vaccine is highly

reactogenic in immune individuals, and can result in induration, sterile abscesses, and necrosis at the

injection site. Sterile abscesses may spontaneously drain or require surgical drainage. Immunologic

screening (skin testing and antibody measurements) must precede administration of the immunization.

However, personnel with reaction to the screening must not be given the vaccine unless approved by a

physician. Vaccine is contraindicated for individuals with positive skin tests and/or antibody titers.

NOTE

A new vaccine prepared by chloroform-methanol extraction is being

evaluated. This vaccine is safe, immunogenic in nonsensitized human

volunteers, and is not reactogenic in sensitized guinea pigs.

c. Post-exposure Chemoprophylaxis. Chemoprophylaxis (tetracycline 500 mg orally every 6

hours for 5 days, or doxycycline 100 mg orally every 12 hours for 5 days) is effective if begun 8 to 12 days

post-exposure.

NOTE

Chemoprophylaxis is not effective if given immediately (1 to 7 days)

post-exposure; it merely delays the onset of disease.

2-51. Biological Warfare Clinical Presentation

a. Incubation. 2 to 14 days (usually 7 days).

b. Signs and Symptoms. See endemic disease, above.
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2-52. Diagnosis

a. Laboratory confirmation is accomplished by serologic testing for antibody titers. Acute Q

fever results in high titers to Phase II antigen and lower antibody titers to Phase I antigen, while the antibody

titers to Phase I antigen is higher during chronic Q fever. An ELISA test for IgM antibody is available at

the USAMRIID and is more sensitive than the standard complement fixation test. A single high titer may be

diagnostic as early as 10 to 14 days into the illness. A four-fold rise in titer in paired acute/convalescent

sera is diagnostic of acute Q fever. Chronic Q fever is confirmed by complement fixation titer of 1:200 or

greater to Phase I antigen. Cultures for C. burnetii are technically difficult, hazardous, and generally not

done. C. burnetii can be identified on biopsy specimens (tissue) by immunofluorescent stain or electron

microscopy. Nonspecific laboratory findings may include leukocytosis in one third of the patients. Mild

elevations of transaminase levels (2 to 3 times the upper limit of normal) are typical. Bilirubin is usually normal.

b. Chest x-ray findings are abnormal in approximately one half of symptomatic cases and may

include pleural effusions in up to 35 percent of cases, nonsegmental and segmented pleural based opacities,

increased interstitial markings, and hilar adenopathy.

c. Differential diagnosis should include the diverse causes of either rapidly progressive or atypical

pneumonia.

2-53. Decontamination

A 0.5 percent chlorine solution should be used for personnel and patient decontamination; the M291 skin

decontaminating kit will not neutralize the organisms. Q fever has been transmitted from heavily

contaminated unwashed laundry; therefore the laundry must be marked and managed as infectious material.

Sputum and urine from patients should be autoclaved before disposal.

2-54. Treatment

a. Triage Categories. Triage categories will vary with the severity of the disease and available

resources. Most patients with Q fever are placed in the Delayed category.

b. Medical Management.

(1) Acute Q fever. While acute Q fever may run a brief, self-limited course without therapy,

suspected cases of acute Q fever should be treated to reduce the risk of development of chronic disease.

Therapeutics for acute Q fever are to

 Administer doxycycline 100 mg orally every 12 hours for at least 2 days after the

patient is afebrile.

 Administer tetracycline 500 mg every 6 hours for at least 2 days after the patient

is afebrile.
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 Consider treating patients unable to take tetracycline with ciprofloxacin and other

quinolones, which are active in vitro. The duration of therapy is usually 5 to 7 days, at least 2 days after the

patient is afebrile. Quinolones are not recommended for the treatment of children.

(2) Chronic Q fever. Therapy for Q fever endocarditis and other forms of chronic Q fever is

complex, controversial, and beyond the scope of this manual. However, recommended regimens have

included doxycycline combined with rifampin, ofloxacin, or TMP/sulfa and continued for at least 2 years.

Antibody titers should be monitored every 6 months during therapy. Monitoring should be continued every

3 months for the first 2 years after therapy. Valve replacement is often necessary to cure Q fever

endocarditis; however, this procedure should be reserved for hemodynamic indications or embolic

complications.

c. Prognosis. Q fever usually results in a self-limited febrile illness of 2 to 14 days in duration.

Previously healthy individuals would be expected to make a complete recovery. Fulminant pneumonia and

chronic Q fever (including endocarditis and neurologic sequelae) are uncommon.

2-55. Control of Patients, Contacts, and Treatment Areas

Q fever is not communicable person to person. Observe Standard Precautions when handling patients.

Unlike most other potential biological weapons, heavy environmental contamination with C. burnetti could

pose a long-term risk due to environmental persistence. Dusts generated from the contaminated environment

may continue to transmit the disease. Exposed clothing and equipment should be decontaminated.

2-56. Medical Evacuation

Patients may be evacuated with other classes of patients.

Section VIII. TULAREMIA

2-57. General

a. Etiologic Agent. Francisella tularensis (F. tularensis) is an aerobic catalase-positive, gramnegative coccobacillus.

b. Reservoir. F. tularensis is maintained in numerous and diverse mammalian (rabbits, hares,

rodents,) and tick reservoirs. F. tularensis is limited to the northern hemisphere. Type A (the predominant

strain in North America) is more virulent than Type B (the predominant strain in Northern Europe).

c. Transmission. Transmission is by arthropod vectors (ticks and deerflies; also mosquitoes in

Sweden, Finland, and the former Soviet Union), direct contact with infected animals, aerosols generated by

skinning/processing infected animals, and ingestion of contaminated food or water. The organisms may

also be transmitted by aerosol as a BW agent.
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d. Endemic Disease.

(1) Clinical syndromes vary with portal of entry, inoculum, strain virulence, and the host’s

underlying state of health. Infection may be subclinical or fulminant. With the exception of typhoidal

tularemia, the clinical syndromes are characterized by the combination of focal processes featuring ulceration

at the portal of entry, and regional adenopathy involving the node groups draining the portal of entry.

Following aerosol exposure, an undifferentiated febrile illness (typhoidal tularemia) or an acute pneumonia

featuring fever, coughing, substernal chest tightness, and pleuritic chest pain may present. Usually,

coughing is nonproductive; hemoptysis is rare. Physical findings may vary. Examination may be normal,

or disclose rales, friction rubs, or findings consistent with consolidation or effusions.

(2) Pharyngeal tularemia presents as an acute pharyngitis following ingestion of contaminated

food or water. The chief complaint is a severe sore throat. Physical findings include fever, exudative

pharyngitis and/or tonsillitis, and possibly pharyngeal ulcers. Also, findings may include a pharyngeal

membrane similar to that seen in diphtheria. Regional adenopathy may present in cervical, preauricular,

and retropharyngeal node groups with occasional abscess formation.

(3) Oculoglandular disease presents following inoculation of the conjunctivae via aerosol,

splashes, or direct contact (contaminated fingers). This disease presents as an acute conjunctivitis and may

feature small conjunctival ulcers or papules. Complications may include corneal ulceration and

dacryocystitis, but visual loss is rare. Regional adenopathy is a conspicuous feature of this illness, with

preauricular or preparotid adenopathy. Severe cases of adenopathy may mimic parotiditis. Differential

diagnosis should include other causes of Parinaud oculoglandular syndrome, including adenovirus infection,

cat scratch disease, syphilis, herpetic infection, and pyogenic bacterial infection.

2-58. Biological Warfare Agent Delivery

The primary threat is by aerosol release, or by contamination of food or water supplies.

2-59. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory analysis and confirmation.

Medical personnel collect medical specimens for supporting laboratory analysis and confirmation.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples for supporting laboratory

analysis and confirmation. Preventive medicine/PHS/BEE personnel collect suspect contaminated water

samples for supporting laboratory analysis and confirmation.

2-60. Prevention

a. Miscellaneous. The military protective mask provides protection of the respiratory tract from

exposure to aerosol organisms. All food must be thoroughly heated before consumption to kill any

organisms. Water must be thoroughly disinfected before consumption.
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b. Pre-exposure Prophylaxis.

• A live attenuated vaccine is available as an IND. It is given by scarification. The

vaccine has been shown to be safe and effective in preventing laboratory-acquired tularemia and experimental

infection in volunteers.

 • The use of ciprofloxacin or doxycycline as a pre-exposure chemoprophylaxis may confer

protection against tularemia, based on in vitro susceptibilities. See paragraph 1-23 for off-label indications

and IND requirements.

c. Post-exposure Prophylaxis. Post-exposure prophylaxis following a BW attack include—

• Administer doxycycline 100 mg orally every 12 hours for 2 weeks; or tetracycline 500

mg orally every 6 hours for 2 weeks; or ciprofloxacin 500 mg orally every 12 hours for 2 weeks.

• Chemoprophylaxis is not recommended following potential natural exposures (tick bite,

rabbit or other animal exposures).

2-61. Biological Warfare Clinical Presentation

a. Incubation. 1 to 21 days (usually 3 to 5 days).

b. Signs and Symptoms. The BW agent presentations of tularemia will be the pneumonic and

typhoidal forms as discussed in paragraph 2-57 above. Oculoglandular disease could possibly occur

following inoculation of the conjunctivae.

2-62. Diagnosis

a. Serologic testing is the preferred procedure for laboratory confirmation. Confirmation of

diagnosis requires a four-fold increase in titer; serologies may need to be repeated at 7 to 10 day intervals.

Agglutination tests and ELISA are also available. A gram stain of expectorated sputum is usually

unrewarding; generally, the organism is not visualized on stains of clinical specimens. Cultures are not

advised for diagnostic purposes. The organism does not grow on standard bacteriologic growth media. F.

tularensis can be cultured on special supportive media containing cystine or another sulfhydryl source.

However, cultures of the organism pose a significant occupational hazard to laboratory personnel. When

cultures for F. tularensis are submitted, laboratory personnel must be alerted, as these cultures must be

processed at Biosafety Level 3. Blood specimens may be submitted for mouse/egg inoculation.

b. Radiographic findings are nonspecific and may include subsegmental or lobar infiltrates,

apical or miliary infiltrates, cavitation, pleural effusions, and hilar adenopathy.

2-63. Treatment

a. Triage Categories. Triage categories will vary according to the severity of the illness,

available resources, and personnel. Patients presenting during the early stages of tularemia pneumonia are
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classified as either Delayed or Immediate depending on the severity of illness and the requirement for

respiratory support.

b. Medical Management. Supportive care may include respiratory support and hydration. Open

lesions should be covered and topical antibiotics applied. Antibiotic therapy may be one of the following:

 Administer streptomycin 7.5 to 10 mg/kg IM every 12 hours for 10 to 14 days.

 Administer gentamicin 3 to 5 mg/kg IV daily for 10 to 14 days.

 Administer ciprofloxacin 400 mg IV every 12 hours, switch to oral ciprofloxacin (500

mg every 12 hours) after the patient is clinically improved; continue for completion of a 10- to 14-day

course of therapy.

 Administer ciprofloxacin 750 mg orally every 12 hours for 10 to 14 days.

c. Prognosis. Inhalation tularemia can lead to fulminant pneumonia with case fatality of 30 to 60

percent without treatment.

2-64. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions. Tularemia is not communicable person to person.

2-65. Medical Evacuation

Patients may be evacuated. Observe Standard Precautions during evacuation.
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CHAPTER 3

VIRAL AGENTS

Section I. INTRODUCTION

3-1. General

Viruses are the simplest type of microorganism and consist of a nucleocapsid protein coat containing genetic

material, either ribonucleic acid (RNA) or DNA. Potential viral BW agents include smallpox, VEE, and VHF.

Section II. SMALLPOX

3-2. General

a. Etiologic Agent. Variola is a member of the poxvirus family and is very contagious to

humans. In addition, some animal poxviruses are virulent to humans (for example, monkeypox).

Theoretically, recombinant poxviruses could be developed from animal poxviruses or vaccinia, and used as

biological weapons.

b. Reservoir. Humans were the only natural reservoir of variola. Variola was eradicated as an

endemic human pathogen, but known laboratory cultures of variola are maintained under security at the

CDC, Atlanta, Georgia, and the State Research Center of Virology and Biotechnology, Koltsovo, Russia.

c. Transmission. Usually occurred by respiratory droplet transmission, following close face-toface contact. Smallpox was also transmitted by direct contact with skin lesions or drainage, or with

contaminated objects. Although uncommon, airborne transmission (long distance) also occurred.

d. Endemic Disease. Smallpox has been eradicated as an endemic disease. The last naturally

acquired reported cases occurred in October 1977, in Somalia. However, if variola is delivered as a BW

agent, it could result in the reemergence of smallpox. Once reestablished as an endemic disease, it could

again be spread by respiratory droplet or droplet nuclei, or by contact with scabs, lesion drainage, and

contaminated objects.

3-3. Biological Warfare Agent Delivery

The primary threat is delivery by aerosol release.

3-4. Environmental Detection

The NBC reconnaissance teams or other bioengineering personnel operating similar detection equipment

accomplish detection.
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3-5. Prevention

a. Pre-exposure Prophylaxis. There are no routine immunizations of US forces for smallpox.

When the threat indicates, senior leadership may direct vaccination of personnel with vaccinia.

NOTE

Contraindications to pre-exposure prophylaxis include pregnancy,

impaired immunity, human immunodeficiency virus (HIV) infection,

eczema, severe burns, psoriasis, other chronic dermatoses, and

individuals with household or other close contacts with the above

conditions.

b. Post-exposure Prophylaxis.

(1) All individuals exposed to or suspected of being exposed to smallpox BW agents should

have active or passive immunization. Contacts that are not immunized or those immunized more than 3

years prior to exposure should be given vaccinia as soon as possible (within 1 to 7 days) following

exposure. Limited data obtained during the era of endemic smallpox suggested that vaccinia combined with

vaccinia immunoglobulin (VIG) was slightly more effective than vaccinia alone for post-exposure

immunoprophylaxis. The combination of vaccinia and VIG is very rational if post-exposure

chemoprophylaxis cannot be given within 7 days of exposure.

(2) With the exception of significant immunodeficiency, there are no contraindications to

vaccinia following smallpox exposure. For contacts with pregnancy or eczema at increased risk for

vaccinia side effects, the combination of vaccinia and VIG 0.6 ml/kg is advised. Vaccinia immunoglobulin

was administered in divided doses at multiple locations over 24 to 36 hours. Patients with HIV infection or

other immunodeficiencies would be candidates for VIG alone.

(3) Possible side effects of vaccinia (vaccinia is a live virus) are the potential to cause disease

in vaccinees and their contacts, especially those with conditions outlined above. Inadvertent inoculation to

skin due to touching or scratching a vaccine lesion and then other areas of skin, and inadvertent inoculation

of the eyes (ocular vaccinia) resulting in an intense conjunctivitis with vesicles and pustules; keratitis and

corneal ulceration could result. Topical antivirals were used anecdotally to treat herpetic ocular infections

(idoxuridine, vidarabine); these agents are active in vitro versus vaccinia.

(4) Generalized vaccinia is a rare idiosyncratic reaction featuring mild constitutional symptoms

and a generalized vesicular rash. Vaccinia cannot be cultured from the vesicles or from the serum of patients

with this condition. Pathogenesis is unknown, but is possibly due to an immunopathologic mechanism.

Usually, this is a self-limited reaction and no therapy is indicated, but VIG may be indicated for severe cases.

(5) Idiosyncratic reactions of varying severity were seen that require supportive care. These

included generalized urticarial exanthems, such as erythema multiforme and Stevens-Johnson syndrome.
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(6) Encephalitis occurs in approximately two individuals per million receiving the vaccine.

This complication produced a case fatality rate of 10 to 30 percent and neurologic sequelae in survivors.

The pathogenesis is unknown but is probably due to an immunopathologic mechanism because vaccinia

cannot be cultured from CSF or brain tissue of patients. Treatment is supportive.

(7) Eczema vaccinatum is a severe dermatitis featuring replication of vaccinia at sites of eczema,

psoriasis, burns, or other chronic or severe cutaneous lesions. Therapy is the administration of VIG 0.6 ml/kg

every 2 to 3 days IM in divided doses at multiple sites over a 24 to 36 hour period until no new lesions appear.

(8) Vaccinia necrosum occurred in immunocompromised vaccinees. This condition featured

an intense local reaction at the site of the vaccination, progressing to local necrosis. The lesion can progress

by local extension and metastasize to distant sites on the skin; it is potentially fatal. Therapy is the

administration of VIG 0.6 ml/kg every 2 to 3 days IM in divided doses at multiple sites over a 24 to 36 hour

period until definite clinical improvement is apparent.

(9) Fetal vaccinia may result from giving vaccinia to females during pregnancy. The

prognosis for the fetus is poor, resulting in stillbirth.

3-6. Biological Warfare Clinical Presentation

a. Incubation Period. The incubation period is 7 to 17 days, commonly 10 to 12 days.

b. Signs and symptoms.

(1) Smallpox begins as a febrile prodrome of 2 to 4 days duration, featuring the acute onset

of fever, rigors, malaise, headache, backache, and vomiting. Other features of the prodrome included

delirium and a transient erythematous macular rash, each occurring in approximately 15 percent of patients.

The characteristic exanthematous phase begins with an acute papular dermatitis on the face, hands, and

forearms, then spreading to the lower extremities and the trunk. Distribution of the rash is centrifugal, with

face and distal extremities involved earlier and to a greater extent than proximal extremities or trunk. The

lesions progress in a synchronous manner from papule to vesicle to pustule. Scabs form in 8 to 14 days and

slough off in 14 to 28 days after the onset of the rash. The sloughing leaves depressed depigmented scars.

Enanthems involving the upper aerodigestive tract may also occur.

(2) Variants include flat-type smallpox, featuring severe systemic toxicity and large flat

maculopapular lesions with a soft, velvety, nonindurated texture. The most severe form of smallpox is the

hemorrhagic variant, featuring severe systemic toxicity, and diffuse ecchymosis and purpura. This variant

is associated with a high-titer viremia and absent or negligible antibody responses; patients usually died

before the characteristic papules or vesicles appeared. A relatively mild form of smallpox (variola minor,

alastrim) featured little systemic toxicity and a milder exanthem and was seen in parts of southern Africa,

Europe, and Latin America. It was due to a less virulent strain of variola.

(3) Complications of smallpox include encephalitis in 1 per 500 cases, with high rates of

mortality and neurologic sequelae among survivors. Keratitis with corneal ulceration leading to blindness
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occurred in 1 percent of cases. Pulmonary edema could complicate the course of hemorrhagic and flattype variants.

3-7. Diagnosis

Differential diagnosis of a vesicular or pustular exanthem may include other infections (varicella,

enteroviruses, rickettsialpox, septicemic melioidosis) or autoimmune diseases (dermatitis herpetiformis,

bullous erythema multiforme, and so forth). Cytologic examination of specimens obtained from the bases

of unroofed vesicles may disclose eosinophilic inclusions (Guarnieri bodies) which are sites of viral

replication in the cytoplasm. Poxviruses may also be identified by electron microscopy of specimens

obtained from skin lesions; however, these methods will not differentiate poxviruses. Clinical specimens

(serum, respiratory secretions, specimens obtained from skin lesions or crusts) may be sent to the laboratory

for culture. The virus may also be cultured from the blood during the prodrome. Poxviruses may be

identified by differential growth characteristics in tissue culture. The use of genetic typing methods will

lead to a specific diagnosis.

3-8. Treatment

a. Triage Category. The triage category varies with conditions and available resources; given

the prolonged incubation, prodrome, clinical course, and lack of specific therapy, most patients should be

categorized as Delayed. Contacts should be vaccinated or receive booster vaccinations as soon as possible,

optimally within 24 hours.

b. Medical Management. Provide supportive care. There is no specific antiviral therapy available

for smallpox.

c. Prognosis. Case fatality rate for smallpox (variola major) was historically 20 to 40 percent

and higher during pregnancy or the neonatal period. Case fatality for the flat-type variant was approximately

95 percent in the unimmunized and 66 percent in previously immunized patients. The hemorrhagic variant

was nearly always fatal. Case fatality for variola minor (alastrim) was 5 percent.

3-9. Control of Patients, Contacts, and Treatment Areas

a. Patients. Strict (standard, contact, and airborne) isolation and quarantine of all patients must

be maintained until scabs have separated. The virus can be spread by air currents and can be carried outside

the hospital by various materials contaminated by the patient, especially clothing and linens. Deposit all

oral and nasal discharges in a paper container and burn. Sterilize (autoclave or boil) all bedclothes and

other fabrics that are exposed to the patient. Spray or mop all floors, walls, and other hard surfaces in the

patient isolation area with a disinfectant solution (phenolic and quaternary ammonium compounds, formalin,

or a 5 percent chlorine solution). Allow the disinfectant to remain on the surfaces for at least 4 hours.

b. Patient Contacts.
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(1) The reappearance of a single case of smallpox would be a global emergency. Immediately

report all occurrences to Military Public Health.

(2) Quarantine all direct contacts with any case and maintain daily surveillance for 17 days

after last known contact with a case. Vaccinate all contacts, including health care workers, if they have not

been immunized or received a booster within 3 years (see post-exposure prophylaxis paragraph 3-5b above).

c. At Risk Personnel. Conduct an epidemiological investigation to identify all potentially exposed

personnel. Quarantine identified personnel for the remainder of the incubation period; usually 7 to 12 days

following the appearance of index cases. Give post-exposure prophylaxis as discussed in paragraph 3-5b above.

3-10. Medical Evacuation

Smallpox is an IQD. Apply strict quarantine measures. Isolate and evacuate all smallpox patients in

cohorts of smallpox patients only. Do not evacuate smallpox patients across national boundaries unless

approved by major command authority (see paragraph 1-21).

Section III. VENEZUELAN EQUINE ENCEPHALITIS

3-11. General

a. Etiologic Agent. The VEE virus is an arthorpodborne alphavirus.

b. Reservoir. Enzootic serotypes are maintained in a rodent-mosquito cycle. Enzootic strains

are frequently transmitted to humans living in endemic disease areas via mosquito bites. However, enzootic

strains are not virulent for horses. Epizootic serotypes are thought to arise from enzootic strains by

mutation. In contrast to enzootic strains, epizootic strains are highly virulent for Equidae (horses, mules,

donkeys). Horses serve as amplifying hosts of epizootic (but not enzootic) strains, providing a source of

virus for mosquitoes, which transmit virus to humans. The VEE virus occurs in northern South America,

Central America, and Trinidad.

c. Transmission. The endemic disease is transmitted by mosquitoes. Aerosol transmission has

occurred in laboratory settings, but is not known to occur naturally.

d. Endemic Disease. The epizootic VEE virus has an incubation period of 1 to 15 days. The

usual presentation is an undifferentiated febrile illness with fever, malaise, and headache. Other symptoms

that may appear include myalgia (72 percent), vomiting (50 percent), drowsiness (40 percent), chills (20

percent), sore throat (20 percent), and diarrhea (20 percent). Fever can remit but recur the following day.

Patients may be incapacitated by malaise and fatigue for 1 to 2 weeks. Less than 1 percent of adults will

develop severe encephalitis featuring meningismus, ataxia, seizures, and coma; paralysis and neurologic

sequelae may result in survivors. The case fatality rate in adults is approximately 1 percent of all cases, but

may reach 10 percent with CNS involvement.
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3-12. Biological Warfare Agent Delivery

The primary threat is delivery by aerosol release.

3-13. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for submission to the supporting medical laboratory

for analysis and field confirmation. Medical personnel will collect specimens from patients presenting at

MTFs with signs and symptoms of the VEE virus (outside of its natural geographic range, it would suggest

a possible BW attack or importation of infected horses or mosquito vectors) for supporting laboratory

analysis and confirmation. Veterinary personnel collect samples from equines within the AO for laboratory

analysis and confirmation. A natural epidemic would usually be preceded by equine disease. A BW attack

will most likely result in human disease as a primary event, or the simultaneous onset of disease in humans and

equines. A BW attack in an area with equines and mosquito vectors may also initiate an epizootic/epidemic.

3-14. Prevention

a. Pre-exposure Prophylaxis. Live attenuated vaccine (TC-83) is available as an IND. However,

20 percent of vaccinees do not respond and another 20 percent develop severe reactions. An inactivated

vaccine (C-84) is available as an IND for TC-83 nonresponders. The C-84 vaccine has the typical

disadvantages of inactivated vaccines (multiple doses and boosters are required to confer and maintain

immunity). In addition, C-84 vaccine does not protect rodents against experimental aerosol challenge;

human data is not available.

b. Post-exposure Prophylaxis. There are no post-exposure prophylaxes available.

3-15. Biological Warfare Clinical Presentation

a. Incubation Period. Incubation period is 1 to 6 days; onset is sudden.

b. Signs and Symptoms. See endemic disease above.

3-16. Diagnosis

Perform serologic tests to measure antibody titers. A single high titer IgM value 5 to 7 days after the onset

of illness is supportive; a four-fold rise in antibody titer in paired acute and convalescent sera is diagnostic.

Identification of the virus in clinical specimens (serum, CSF) by PCR is under investigation. Viral cultures

may confirm the diagnosis if serum is sent early during the illness (a low titer viremia is present during the

first 24 to 72 hours of illness); however, cultures will be negative later in the clinical course and in those

who have progressed to encephalitis. Nonspecific laboratory findings include lymphopenia, and
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occasionally, neutropenia and mild thrombocytopenia. Transaminase levels (aspartate aminotransferase and

lactate dehydrogenase) are usually elevated and a CSF lymphocytic pleocytosis may be present.

3-17. Treatment

a. Triage Categories. The triage categories vary according to severity of the disease and available

resources. Most patients are placed in the Delayed category, given the usual clinical course and a lack of

specific therapy. Patients with seizures are placed in the Immediate category for anticonvulsive therapy,

airway management, and other supportive care measures.

b. Medical Management. There is no specific antiviral therapy. Administer anticonvulsive

therapy for patients with seizures and other supportive care measures as indicated.

c. Prognosis. The VEE virus is an incapacitating agent. While acute morbidity is severe,

most patients recover. However, animal studies demonstrate that aerosol exposure leads to viral

attachment to olfactory nerve endings and direct invasion of the CNS via the olfactory nerve, resulting in

a high incidence of CNS disease. This suggests that in contrast to the mosquito-borne disease, VEE

resulting from a BW attack would be more likely to cause CNS involvement and could be associated with

higher morbidity and mortality.

3-18. Control of Patients, Contacts, and Treatment Areas

a. Patient Management. Apply Standard Precautions for infection control.

b. Management of Patient Contacts. Observe Standard Precautions. Control mosquito vectors

and vaccinate horses in the vicinity. The VEE virus is not communicable person to person.

3-19. Medical Evacuation

Patients may be evacuated with all other classes of patients.

Section IV. VIRAL HEMORRHAGIC FEVERS

3-20. General

a. Etiologic Agent. The VHF viruses belong to four families of lipid-enveloped viruses with

single-stranded RNA genomes. The taxonomy, ecology, and epidemiology of these viruses are summarized

below. Transmission of VHFs varies with the specific virus. However, all of the VHFs, with the exception

of dengue, are potentially transmitted via aerosol, underscoring their possible role as BW agents. Table 3-1

provides the taxonomy of VHFs.
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Table 3-1. Taxonomy of Viral Hemorrhagic Fevers

VIRUS DISEASE GEOGRAPHY RESERVOIR TRANSMISSION

ARENAVIRIDAE

NEW WORLD COMPLEX

JUNIN ARGENTINE VHF S. AMERICA RODENT AEROSOL, FOMITES

MACHUPO BOLIVIAN VHF S. AMERICA RODENT AEROSOL, FOMITES

GUANARITO VENEZUELAN VHF S. AMERICA RODENT AEROSOL, FOMITES

SABIA BRAZILIAN VHF S. AMERICA UNKNOWN AEROSOL, FOMITES

OLD WORLD COMPLEX

LASSA BUNYAVIRIDAE LASSA FEVER W. AFRICA RODENT AEROSOL, FOMITES

PHLEBOVIRUS GENUS

RIFT VALLEY RIFT VALLEY FEVER AFRICA MOSQUITO MOSQUITO, AEROSOL

OR FOMITES FROM

SLAUGHTERING

INFECTED ANIMALS

NAIROVIRUS GENUS CRIMEAN-CONGO VHF AFRICA, TICKS MOSQUITO, AEROSOL

MIDDLE EAST, OR FOMITES FROM

E. EUROPE SLAUGHTERING

INFECTED ANIMALS

HANTAVIRUS GENUS

HANTAAN VHF WITH RENAL SYNDROME ASIA, EUROPE RODENT AEROSOL, FOMITES

DOBRAVA VHF WITH RENAL SYNDROME E. EUROPE RODENT AEROSOL, FOMITES

SEOUL VHF WITH RENAL SYNDROME WORLDWIDE RODENT AEROSOL, FOMITES

PUUMALA NEPHROPATHIA ENDEMICA EUROPE RODENT AEROSOL, FOMITES

FILOVIRIDAE FAMILY

EBOLA EBOLA VHF AFRICA, ASIA UNKNOWN UNKNOWN

MARBURG MARBURG VHF AFRICA UNKNOWN UNKNOWN

FLAVIVIRIDAE FAMILY

MOSQUITO-BORNE

YELLOW FEVER YELLOW FEVER S. AMERICA, MOSQUITO, MOSQUITO

AFRICA PRIMATE

DENGUE DENGUE, DENGUE VHF TROPICS AND MOSQUITO, MOSQUITO

SUBTROPICS HUMANS

TICK-BORNE

KYASANUR FOREST KYASANUR FOREST DISEASE INDIA RODENT, MONKEY TICK

OMSK OMSK VHF SIBERIA RODENT TICK

b. Endemic Disease. Viral hemorrhagic fever is a clinical syndrome featuring fever, myalgia,

malaise, and hemorrhage, and in some cases, hypotension, shock, and death. Viral pathogenesis is complex,

incompletely understood, and varies among specific viruses. Some infections result in immune complex

deposition which activates complement and other inflammatory cascades. This process damages vascular

endothelium, results in capillary leak, and deregulates vascular smooth muscle tone. These lead to

hypotension, shock, and end-organ failures. Some of these diseases activate coagulation cascades and result

in DIC. Hemorrhage can also be enhanced by specific end-organ failures. For example, yellow fever can

cause massive hepatic necrosis resulting in a deficiency of vitamin K-dependent clotting factors. The uremia
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complicating the acute renal failure of hemorrhagic fever with renal syndrome (HFRS) leads to platelet

dysfunction, further promoting hemorrhage. The final common pathway of hemorrhagic fever is damage to

the vascular endothelium.

3-21. Biological Warfare Agent Delivery

The primary threat is delivery by aerosol release.

3-22. Environmental Detection

The NBC reconnaissance teams collect environmental samples for submission to the supporting medical

laboratory for analysis. Preventive medicine/PHS/BEE personnel collect water samples for laboratory analysis.

Veterinary personnel collect blood samples from animals for laboratory analysis. Medical personnel collect

blood and other specimens from patients presenting with signs and symptoms for laboratory analysis.

3-23. Prevention

a. Pre-exposure Prophylaxis. For pre-exposure prophylaxis, ensure all service members have

received their yellow fever vaccinations. Investigational vaccines are available as INDs. Argentine

hemorrhagic fever (AHF) attenuated vaccine has been safely used and has proven effective in preventing

AHF in more than 150,000 agricultural workers in endemic areas; animal studies suggest that this vaccine

also provides protection against Bolivian VHF. Two Rift Valley hemorrhagic fever vaccines (an inactivated

vaccine and a live attenuated vaccine) are in development.

b. Post-exposure Chemoprophylaxis. As a post-exposure chemoprophylaxis, administer ribavirin,

500 mg orally every 6 hours for 7 days, for Crimean-Congo VHF (CCVHF) and Lassa fever. Ribavirin

(intravenous and oral) is available under IND status and available through human use protocol only.

3-24. Biological Warfare Clinical Presentation

a. Incubation Period. The incubation period can be days to months.

b. Signs and Symptoms. Initial clinical features may include flushing, conjunctival injection,

possible periorbital edema, petechiae, and hypotension. Illness then progresses with prostration, fatigue,

and hemorrhage. The most dreaded complications are shock, multiple organ system failure, and death.

3-25. Diagnosis

Serologic methods include IgM antibody capture and ELISA techniques to detect the antigen. Tissue can be

submitted for immunohistochemical staining, electron microscopy, or for genetic typing. Serum and other

clinical specimens should be forwarded for viral culture under maximum containment (Biosafety Level 4).
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Laboratory findings are nonspecific and variable. In general, these result in thrombocytopenia and

leukopenia. Elevated liver function tests and other nonspecific laboratory findings may be present. The

blood urea nitrogen (BUN) will be related to the circulatory status with the exception of HFRS in which the

kidneys are target organs of the Hantaviruses. Differential diagnosis include diseases such as typhoid fever,

meningococcemia, leptospirosis, malaria, vasculitic diseases, hemolytic uremic syndrome, thrombotic

thrombocytopenic purpura, and the diverse etiologies of DIC.

3-26. Treatment

a. Triage Categories. The triage categories vary according to the severity of disease and available

resources. Patients who are acutely ill with AHF, Bolivian VHF, Brazilian VHF, Venezuelan VHF, Lassa

fever, CCVHF, or HFRS may be candidates for the Immediate category if ribavirin is available, as ribavirin

may improve outcome. If ribavirin is not available, these patients are placed in the Delayed category.

Other patients with hemorrhagic fevers may be classified as Delayed or Expectant categories.

b. Medical Management.

(1) Treatment is primarily supportive with special attention to fluid and electrolyte balance.

Patients require treatment for shock, blood loss, renal failure, seizures, and coma. Treatment may include

intensive care and specific interventions such as mechanical ventilation, dialysis, and neurological support.

Heparin therapy may provide benefit for DIC. However, its role is controversial and should be reserved for

patients with clinically significant hemorrhage and laboratory evidence of DIC. Aspirin and other

medications that impair platelet function are contraindicated; as are IM injections. The use of intravascular

devices must be carefully considered in the context of potential benefit versus the risk of hemorrhage.

Surgical interventions should not be withheld if indicated.

(2) Specific antiviral therapy is limited. Clinical studies support the use of IV ribavirin for

the treatment of Lassa fever and HFRS (Hantaan virus). The role of ribavirin therapy for CCVHF is

supported by in vitro studies, although there is no clinical experience. Ribavirin (IV and oral) is available

under IND status and is available through human use protocol only. For Lassa fever and CCVHF, administer

a loading dose of ribavirin 30 mg/kg IV, followed by 16 mg/kg IV every 6 hours for 4 days; then 8 mg/kg IV

every 8 hrs for 6 days to complete a 10-day course of therapy. For HFRS, therapy may benefit patients who have

been febrile for 6 days or less. Administer a loading dose of ribavirin 33 mg/kg IV, followed by 16 mg/kg IV

every 6 hours for 4 days, then 8 mg/kg IV every 8 hours for 3 days, to complete a 7 day course of therapy.

c. Prognosis. Prognosis varies from agent to agent; case fatality rates range from less than 10

percent (HFRS) to as high as 90 percent (Ebola). Survivors may be left with long-term sequelae (such as

blindness, neurosensory hearing loss, and other neurologic, retinal, and ocular involvement).

3-27. Control of Patients, Contacts, and Treatment Areas

a. Report. Report suspected cases of VHFs outside the US to PVNTMED/PHS personnel

immediately. Yellow fever is an IQD.
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b. Isolation. The following recommendations apply to patients with suspected or proven

arenavirus, filovirus, or CCVHF virus infections: these patients should be isolated in private rooms or

isolation tents; if private rooms are not available, only other patients with the same disease should be in the

same room; a negative air flow room should be used, if possible, if the patient has significant cough,

hemorrhage, or diarrhea. Limit exposure to caregivers only; other staff members and visitors should not

be allowed in the room to avoid injuries/nosocomial exposures. Caregivers should be the most skilled/

experienced staff.

c. Caregiver Protection. The following recommendations apply to patients with suspected or

proven arenavirus, filovirus, or CCVHF virus infections: all caregivers must wear gloves and gowns;

anyone coming within 3 feet of the patient should also wear face shields or surgical masks and eye

protection (for example, goggles or eyeglasses with side shields). When caring for patients with prominent

cough, vomiting, diarrhea, or hemorrhage, caregivers should wear a HEPA filter air purifying respirator, a

battery powered, air-purifying respirator, or a positive pressure supplied air respirator.

d. Infectious Material Handling. Sewage, bulk blood, suctioned fluids, secretions, and excretions

should be autoclaved, processed in a chemical toilet, or treated with a 5 percent chlorine solution for at least

5 minutes in bedpan or commode prior to flushing.

e. Contacts.

(1) Casual contacts. There is no known risk of transmission to casual contacts, such as

travelers in the same airplane.

(2) Close contacts. Close contacts, such as household members, physicians, nursing care,

and individuals handling laboratory specimens, increase the possibility of contracting the disease. Close

contacts should have their temperature recorded twice daily for 3 weeks post-exposure. Close contacts

should receive post-exposure chemoprophylaxis/evaluation/treatment if fever (above 101°F) or other

systemic symptoms present within 3 weeks of exposure.

(3) High-risk contacts. High-risk contacts include anyone who has mucous membrane or

percutaneous exposures. High-risk contacts with mucous membrane exposure should copiously irrigate

with water or eyewash solution for at least 15 minutes. For percutaneous exposure, individuals should

frequently wash affected skin surfaces with soap and water; an antiseptic solution or handwashing agent

may also be considered to provide better removal of any contamination on the exposed surfaces. High-risk

contacts with exposure to Lassa fever and CCVHF should

 Receive post-exposure chemoprophylaxis (ribavirin 500 mg orally every 6 hours

for 7 days).

 Have their temperature recorded twice daily for 3 weeks post-exposure.

 Receive further evaluation/treatment if fever (greater than 101°F) or other systemic

symptoms present within 3 weeks of exposure.
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3-28. Medical Evacuation

Evacuation may result in increased morbidity and mortality for patients with VHFs; therefore, treatment at

a local facility is preferred. Strict isolation as outlined in paragraph 3-27 above must be used for all patients

evacuated. Obtain approval from the senior medical authority before evacuation; see paragraph 1-21 for

more information.
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CHAPTER 4

TOXINS

Section I. INTRODUCTION

4-1. General

Toxins are poisonous byproducts of living organisms. They are very stable and produce severe illness when

ingested, inhaled, or introduced into the body by any other means. Some toxins are susceptible to heat,

while others are heat stable. Their effects on the human body range from minor illness to death.

Section II. CLOSTRIDIUM BOTULINUM TOXIN

4-2. General

a. Etiologic Agent. Botulinum toxins are a group of seven toxins produced by Clostridium (C.)

botulinum. The spores are ubiquitous; they germinate to give rise to vegetative bacteria that produce toxins

during anaerobic incubation. Industrial-scale fermentation can produce large quantities of toxin for use as a

BW agent. There are three forms of naturally occurring botulismfoodborne, infantile, and wound.

Botulinum toxin is the most potent neurotoxin known; paradoxically it has been used therapeutically to treat

spastic conditions (strabismus, blepharospasm, torticollis, and tetanus). Botulinum toxin consists of two

polypeptide subunits (A and B chains). The B subunit binds to a receptor on the axons of motor neurons.

The toxin is taken into the axon, where the A chain exerts its cytotoxic effect; it inactivates the axon,

preventing release of acetylcholine and neuromuscular transmission (pre-synaptic inhibition). Recovery

follows only after the neuron develops a new axon, which can take months. The presynaptic inhibition

affects both autonomic (muscarinic) and motor (nicotinic) receptors.

b. Reservoir. The reservoir is soil, animals, and fish. The organisms can be recovered from

honey and other agricultural products. High-risk foods are primarily improperly canned foods and dried

meat or fish.

c. Transmission. Consumption of food contaminated with the C. botulinum toxin.

d. Endemic Disease.

(1) Foodborne. Foodborne botulism is due to ingestion of food contaminated with botulinum

toxins. Inadequately heating vegetables and fruits during canning, then inadequate heating before serving is

the primary mode of transmission in the US. In some foreign countries, smoked sausage, salmon, and

fermented salmon eggs are the source of intoxication. In Asian countries, seafood is the primary source of

intoxication.

(2) Infantile. Germination of spores leading to colonization and toxin production may occur

in the infantile GI tract due to anatomic, physiologic, and microbiologic factors present during the first year
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of life. Clostridium botulinum spores survive transit through the stomach in infants, relative to achlorhydria;

spores can then germinate and colonize the intestinal tract in the absence of well-established GI tract

microflora. Parents are advised not to feed infants honey, molasses, and other foods potentially high in C.

botulinum spore content to prevent this disease. This form of botulism is a rare disease of adults, but may

occur in cases of underlying anatomic or physiologic abnormalities of the GI, or alteration of the normal GI

tract flora (such as after antibiotic exposure).

(3) Wound. Wound botulism is due to the germination of C. botulinum spores and in-situ

toxin production in traumatic wounds. The spores may be introduced by organisms entering during

wounding, by drug abusers through subcutaneous injection sites, and by cocaine abusers inhaling the spores

into ischemic nasal ulcers and sinuses.

Botulism can feature milder presentations limited to cranial nerve palsies and mild GI symptoms related to

autonomic dysfunction. Botulism should be considered in the differential diagnosis of patients presenting

with symptoms of cranial nerve neuropathies, especially if numerous patients present simultaneously.

4-3. Biological Warfare Agent Delivery

The primary threat is delivery by aerosol release. Inhalation challenge does not occur naturally, but can be

used in a BW attack. Aerosol dispersion has delivered lethal intoxication to experimental animals. The BW

agent may also be delivered through contaminated food or water.

4-4. Environmental Detection

The NBC reconnaissance teams collect aerosol samples. Veterinary/PHS/PVNTMED personnel collect

food samples for laboratory analysis. Veterinary personnel collect animal specimens for laboratory testing.

Preventive medicine/PHS/BEE personnel collect water samples for laboratory testing. Patient care personnel

collect medical specimens for laboratory testing.

4-5. Biological Warfare Clinical Presentation

a. Incubation. The incubation period for foodborne botulism is usually 24 to 36 hours. The incubation

period for infantile botulism is unknown. The incubation period for wound botulism is usually 3 or more days.

b. Signs and Symptoms.

(1) The autonomic features of botulism are typical anticholinergic signs and symptoms: dry

mouth, ileus, constipation, and urinary retention. Nausea and vomiting may occur as nonspecific sequeli of

ileus. Dilated pupils (mydriasis) occur in approximately 50 percent of cases.

(2) The motor complications of botulism feature a descending paralysis, usually beginning

with cranial nerve palsies leading to blurred vision, diplopia, dysphonia, and dysphagia. Collapse of the upper
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airway may occur due to weakness of the oropharyngeal musculature. As the descending motor weakness

involves the diaphragm and accessory muscles of respiration, respiratory failure may occur.

(3) Sensory symptoms usually do not occur. Botulinum toxins do not cross the blood/brain

barrier and do not cause CNS disease. However, the psychological sequelae of botulism may be severe and

require specific intervention.

(4) Symptoms usually begin 12 to 36 hours following intoxication; time can vary according

to the amount of toxin absorbed and could be reduced to hours following a BW attack.

4-6. Prevention

a. Pre-exposure Prophylaxis. A pentavalent (types A, B, C, D, and E) toxoid vaccine has been

developed as a pre-exposure prophylaxis. This vaccine is safe and effective in animal studies, and has been

demonstrated to be safe in human volunteers. The vaccine remains under an IND status since it is not

feasible to test for efficacy in humans. Vaccine is given by deep subcutaneous injection at 0, 2, and 12

weeks, with a booster 1 year after the initial dose.

b. Post-exposure Prophylaxis. Currently, post-exposure prophylaxis is not available. Animal

experiments demonstrate that botulinum antitoxin is effective; however, human data or practice guidelines

are not available. Botulinum antitoxin should be considered in extraordinary circumstances.

4-7. Diagnosis

Botulism is primarily a clinical diagnosis. Laboratory confirmation may be obtained by the use of an

ELISA test to detect toxin antigen. The assay may be used to test specimens of implicated food or water, or

samples obtained from the environment. Clinical specimens submitted for study may include serum, gastric

aspirates, stool, and respiratory secretions. A simple bioassay (mouse neutralization) confirms the diagnosis

if an aliquot of the patients serum produces descending paralysis when injected into a laboratory mouse.

Nerve conduction studies and single-fiber electromyography (EMG) can confirm the diagnosis, although

these modalities may not be readily available in a tactical setting. Edrophonium test results can be positive

in botulism as well as in myasthenia gravis; therefore, this test may not be useful due to the lack of

specificity. Antibody tests are not useful for botulism, as the amount of antigen required to stimulate an

antibody response exceeds the lethal dose.

4-8. Treatment

a. Triage Categories. Triage categories will vary according to situation and available resources.

Given that up to 95 percent of patients will survive with supportive care, prompt respiratory support and

medical evacuation for further supportive care can be lifesaving. Patients with upper airway compromise

could be placed in the Immediate category. Patients with mild or gradually progressive symptoms could be
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placed in the Delayed category. Patients with respiratory failure due to neuromuscular involvement may be

placed in the Immediate category if endotracheal intubation and respiratory support are available, or in the

Expectant category if these are not available. The implications of a mass casualty situation create a demand

for limited respiratory support resources that are ominous.

b. Medical Management. Supportive care includes respiratory support, hydration, bowel, bladder

and skin care, nasogastric suctioning for ileus, physical therapy, and psychological support. Long-range

issues include meticulous attention to the details of daily care; specifically, the prevention of decubitus

ulcers, nosocomial infections, and deep venous thrombosis.

(1) Specific therapy for inhalation or foodborne/waterborne botulism consists of giving

botulinum antitoxin to neutralize the circulating toxin in patients with progressive symptoms, or who have

not progressed to a stable state. The standard product is a trivalent (types A, B, E) equine antiserum. The

serum is available through CDC. Since this is a horse-derived product, potential complications include

acute (anaphylaxis) and delayed (serum sickness) hypersensitivity reactions. A despeciated equine

heptavalent antitoxin (types A, B, C, D, E, F, G) has been prepared by cleaving the Fc fragments, leaving

F(ab)2 fragments. This product is available through USAMRIID as an IND. The despeciated product has

been effective in animal studies. However, 4 percent of horse antigens are retained; there is still a risk of

hypersensitivity reactions. Administration of either product must be given in an MTF where personnel and

equipment are available to treat possible anaphylaxis. Before administrating the antitoxin, perform a

sensitivity skin test by intradermally injecting 0.1 ml of a 1:10 dilution of antitoxin and monitoring the

patient for 20 minutes. If the injection site becomes hyperemic (greater than 0.5 centimeters [cm] in

diameter), or if the patient develops fever, chills, hypotension, rash, respiratory difficulties, nausea,

vomiting, or generalized pruritus, the test is considered positive. If no allergic symptoms are observed,

administer the antitoxin by IV (10 cubic centimeters [cc] over 20 minutes). Repeat this dose until there is no

more improvement. For patients with positive skin tests, attempt desensitization by subcutaneously

administering 0.01 to 0.1 ml of antitoxin, gradually increase the dose every 20 minutes until 2.0 cc can be

sustained without a marked reaction. Preferably, desensitization should be performed by an experienced

allergist. Medical personnel attempting to give the antitoxin should be prepared to treat a possible

anaphylactic reaction; intubation equipment, epinephrine, and IV access must be immediately available.

(2) Therapy for wound and sinusitis consists of debridement and administration of antibiotics.

NOTE

Aminoglycosides and clindamycin may further impair neuromuscular

transmission and may lead to clinical deterioration if used for patients

with botulism.

c. Prognosis. Botulism can result in severe morbidity. Complications include descending

paralysis, with possible respiratory failure. Case fatality is approximately 60 percent without respiratory

intensive care. However, with respiratory supportive care, prognosis is favorable, with case fatality rates at

approximately 5 percent. Recovery may be prolonged, requiring up to three months for signs of initial
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improvement and up to one year for complete symptomatic recovery. Psychological sequelae may be

severe and require specific interventions.

4-9. Control of Patients, Contacts, and Treatment Areas

The patient can be evacuated. Employ Standard Precautions; botulism is not communicable person to person.

4-10. Medical Evacuation

Patients may be evacuated with other classes of patients. Observe Standard Precautions for evacuation.

Section III. CLOSTRIDIUM PERFRINGENS TOXINS

4-11. General

a. Etiologic Agent. Clostridium perfringens is a common anaerobic bacillus that produces at least

12 toxins. Spores survive cooking and then germinate and multiply at storage at ambient temperature, slow

cooling, or inadequate rewarming. A high inoculum (greater than 100,000 colony-forming units [CFU]/gm

of food) is usually required to produce disease.

b. Reservoir. The reservoir is soil and the GI tract of healthy persons and animals.

c. Transmission. Gas gangrene results from wound contamination with soil containing spores of

C. perfringens. Clostridial food poisoning follows ingestion of foods contaminated with soil or feces and

then stored under conditions that allow replication of the organism.

d. Endemic Disease. The diseases produced by these toxins depend upon the site of C. perfringens

colonization or infection and toxin production. For example, wound infection results in gas gangrene,

while ingesting contaminated food results in clostridial food poisoning, or in susceptible hosts, enteritis

necroticans. Clostridial food poisoning is usually a brief, self-limited disease, featuring the abrupt onset of

nausea, abdominal colic, and diarrhea; vomiting and fever are rare. Individuals can develop gas gangrene

by having wounds contaminated with soil containing bacterial spores. The spores germinate, resulting in

bacterial toxin production. Gas gangrene (clostridial myonecrosis) features necrosis of skeletal muscle and

overlying soft tissue and constitutes a surgical emergency.

4-12. Biological Warfare Agent Delivery

The primary threat is delivery of C. perfringens alpha toxin as an aerosol to the respiratory tract. This would

result in pulmonary disease, vastly different from the naturally occurring diseases associated with C. perfringens.

The toxin may also be delivered in combination with other toxins to produce a variety of clinical effects.
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4-13. Environmental Detection

The NBC reconnaissance teams collect environmental samples for submission to the supporting medical

laboratory for analysis. Medical personnel collect pulmonary secretions from patients presenting with signs

and symptoms for laboratory analysis.

4-14. Prevention

There is no pre-exposure or post-exposure prophylaxis for C. perfringens.

4-15. Biological Warfare Clinical Presentation

a. Incubation. The incubation period is 1 to 6 hours.

b. Signs and Symptoms. Aerosol challenges of C. perfringens alpha toxin produce lethal

pulmonary disease in laboratory animals. The C. perfringens alpha toxin is a highly toxic phospholipase,

which will result in severe injury to the exposed respiratory tract. An aerosol delivery can produce a severe

pulmonary capillary leak, resulting in adult respiratory distress syndrome (ARDS) and respiratory failure.

Absorbed toxin can lead to intravascular hemolysis, thrombocytopenia, and liver damage.

4-16. Diagnosis

Acute serum and tissue specimens should be collected and transported to the designated reference laboratory

for toxin immunoassay. Clinical laboratory findings could include anemia, thrombocytopenia, abnormal

liver function tests, and hypoxia. The differential diagnosis should include other causes of ARDS including

chemical warfare (CW) agent (phosgene or mustard) exposure, inhalation injury due to ricin or

staphylococcal enterotoxin B (SEB), Hantavirus pulmonary syndrome, and other diverse etiologies of

ARDS. Pulmonary disease due to SEB will be less severe; also hemolysis, thrombocytopenia, or liver

damage should not occur.

4-17. Treatment

a. Triage Categories. Triage categories will vary according to severity and stage of illness and

available resources.

b. Medical Management. Medical management consist of supportive care. Patients may require

assisted ventilation to relieve the respiratory effects. There are no specific antitoxins or antidotes available

c. Prognosis. Prognosis is poor.

4-18. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in patient care. The C. perfringens toxin is not communicable person to person.
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4-19. Medical Evacuation

Patients may be evacuated. Apply Standard Precautions during evacuation.

Section IV. RICIN

4-20. General

a. Etiologic Agent. Ricin is a potent cytotoxin derived from the beans of the castor plant (Ricinus

communis). Over one million tons of castor beans are processed annually in the production of castor oil,

which is used for medicinal and industrial purposes including the production of aircraft and marine engine

lubricants, dyes, and paints. The waste mash from this process is approximately 5 percent ricin by weight.

Consequently, large quantities of ricin are easily and inexpensively produced. Ricin consists of two

hemagglutinins and two toxins. These toxins are dimers consisting of cytotoxic A chains and B chains

which serve as transport peptides and bind to cellular membrane receptors. Ricin toxins are potent

inhibitors of DNA replication and protein synthesis. The toxin can be transmitted through contaminated

food and water, percutaneously via small pellets/projectiles designed to carry toxins, or as a BW aerosol.

b. Reservoir. Castor beans.

c. Transmission. Transmission has been by inhalation of organism during industrial operations.

Also, transmitted through ingestion of castor bean meal.

d. Endemic Disease. There is no endemic disease; however, there have been exposures in

industrial operations. Clinical features vary according to the route of intoxication and toxin dose. Accidental

sublethal aerosol exposures occurred during the 1940s. Patients presented with acute onset of fever, chest

tightness, cough, dyspnea, nausea, and arthralgias 4 to 8 hours after exposure. The onset of profuse

sweating several hours later was the sign of termination of most of the symptoms. Lethal aerosol exposures

in humans have not been reported; however, large aerosol exposures in experimental animals result in

necrosis of upper and lower respiratory epithelium, and perivascular and alveolar edema. Respiratory tract

exposure to a large dose will produce necrosis of the entire exposed respiratory tract; pulmonary capillary

leaks result in extravasation of protein-rich fluid into the alveoli, resulting in pulmonary edema, ARDS, and

respiratory failure. Ingestion results in necrosis of the GI epithelium, local hemorrhage, and hepatic,

splenic, and renal necrosis. Intramuscular injection results in severe local muscle necrosis and visceral

organ involvement.

4-21. Biological Warfare Agent Delivery

The primary threat is delivery of the BW agent by aerosol release. Ricin is less toxic than botulinum. A

larger quantity is required to cover a significant area on a battlefield. This feature may limit the use of ricin

as a tactical weapon; however, it can be used for small-scale operations. The agent may also be delivered

through contamination of food and water supplies.
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4-22. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory identification. Preventive

medicine/PHS/BEE personnel collect suspect contaminated water samples for laboratory identification.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples. Veterinary personnel

collect specimens from government-owned animals for supporting laboratory identification. Medical

treatment personnel collect specimens from patients presenting with signs and symptoms for laboratory

identification. The supporting laboratory performs an antigen detection (ELISA) test to identify the presence

of toxins in samples or specimens.

4-23. Prevention

a. Pre-exposure prophylaxis is not available; however, candidate vaccines are under development.

b. Post-exposure prophylaxis is not available.

4-24. Biological Warfare Clinical Presentation

a. Incubation Period. The incubation period is 18 to 24 hours.

b. Signs and Symptoms. See endemic disease, paragraph 4-20.

4-25. Diagnosis

Serum and respiratory secretions may be submitted for antigen detection (ELISA). Immunohistochemical

stains of tissue may also be available. Paired acute and convalescent sera for antibody studies can be

submitted from survivors. Nonspecific laboratory and radiographic findings may include neutrophilic

leukocytosis, bilateral interstitial infiltrates compatible with noncardiogenic pulmonary edema. Differential

diagnosis of respiratory disease would include phosgene exposure, SEB, Hantavirus pulmonary syndrome,

atypical pneumonias including Q fever and tularemia, and diverse causes of ARDS.

4-26. Treatment

a. Triage Categories. Triage categories will vary according to severity of illness and available

resources. Respiratory distress would result in placement of the patient in the Immediate category if

respiratory support was available, or Expectant if respiratory support was not available. Patients with

milder presentations would be candidates for the Delayed category.

b. Medical Management.

(1) Supportive care including intensive care measures, such as supplemental oxygen,

endotracheal intubation and mechanical ventilation, positive end-expiratory pressure, and hemodynamic

monitoring, may be required for respiratory disease.
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(2) Gastrointestinal intoxication is best managed by vigorous gastric decontamination with

lavage and superactivated charcoal, followed by use of cathartics such as magnesium citrate. Volume

replacement of GI tract fluid loss is important.

(3) In percutaneous exposures, treatment would be primarily supportive, managing specific

organ system failures.

(4) Specific therapeutic drugs are not currently available.

c. Prognosis. Prognosis depends on the route and intensity of exposure. Due to a lack of data,

specific prognosis outcomes cannot be stated.

4-27. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in patient care. Ricin is not communicable person to person.

4-28. Medical Evacuation

Patients may be evacuated.

Section V. SAXITOXIN

4-29. General

a. Etiologic Agent. Saxitoxin is the parent compound of a group of related neurotoxins produced

by marine dinoflagellates of the genus Gonyaulax.

b. Reservoir. Shellfish.

c. Transmission. Saxitoxin is transmitted to humans by ingesting bivalve mollusks, which

accumulate dinoflagellates during filter feeding.

d. Endemic Disease. Paralytic shellfish poisoning (PSP) is a severe, life-threatening

neuromuscular condition. Saxitoxin is rapidly absorbed from the GI tract following ingestion of

contaminated shellfish. Saxitoxin binds to the sodium channels of nerve and muscle tissue, preventing

propagation of action potentials in excitable cells. This leads to neuromuscular dysfunction, and in severe

cases, death due to respiratory paralysis and respiratory failure. In contrast to botulism, sensory and CNS

symptoms are present in addition to motor symptoms. Symptoms begin as early as 10 minutes to several

hours after ingestion, depending on the ingested dose and host factors. Initial symptoms include numbness

and tingling of the lips, tongue, and fingertips; followed by numbness of the neck and extremities and motor
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incoordination. Cranial nerve involvement can result in diplopia, speech, and swallowing difficulties.

Other symptoms may include light-headedness, dizziness, weakness, confusion, memory loss, and headache.

Flaccid paralysis and respiratory failure are life-threatening complications, and occur within 2 to 12 hours

after ingestion. The toxin is rapidly cleared by renal excretion; however, complete neurologic recovery

may require 7 to 14 days.

4-30. Biological Warfare Agent Delivery

The primary threat is delivery by aerosol release. Saxitoxin may also be delivered by projectiles or by

contamination of food and water. Contamination of food and water supplies would be on a very limited

basis.

4-31. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory identification. Preventive

medicine/PHS/BEE personnel collect suspect contaminated water samples for laboratory identification.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples. Veterinary personnel

collect specimens from government-owned animals for supporting laboratory identification. Medical

treatment personnel collect specimens from patients presenting with signs and symptoms for laboratory

identification.

4-32. Prevention

a. Pre-exposure Prophylaxis. There is no pre-exposure prophylaxis available. Avoidance of

potentially contaminated food and water will protect individuals from the effects of ingested toxins.

b. Post-exposure Prophylaxis. There is no post-exposure prophylaxis available.

4-33. Biological Warfare Clinical Presentation

a. Incubation. Minutes to hours.

b. Signs and Symptoms. Clinical features would be similar to those discussed above for endemic

disease; animal experiments using aerosol challenges suggest that the clinical course following inhalation is

accelerated and that death occurs within minutes following exposure.

4-34. Diagnosis

Diagnosis is confirmed by antigen (toxin) detection by ELISA test or mouse bioassay. Clinical specimens

which may be submitted for toxin assay include stomach contents, serum, and in a BW context, respiratory
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secretions. Specific toxins can be identified by high-pressure liquid chromatography. Routine clinical

laboratory findings are not specific for saxitoxin poisoning. Cardiac conduction disturbances may develop;

however, these electrocardiographic findings are nonspecific. The differential diagnosis of saxitoxin

poisoning includes ciguatoxin (ciguatera) and tetrodotoxin ingestion. Ciguatoxin occurs following ingestion

of large finned reef fish, and in contrast to saxitoxin, will result in more severe GI symptoms (nausea,

vomiting, diarrhea), and in a peculiar reversal of temperature sensationhot feels cold, cold feels hot.

4-35. Treatment

a. Triage Categories. Triage categories vary according to the severity of the disease and

availability of resources. Following aerosol delivery or toxic projectile, patients may be considered

candidates for the Immediate category for airway and ventilatory support, if available; or candidates for the

Expectant category in remote, isolated locations.

b. Medical Management. Supportive care is essential. Airway management and mechanical

respiratory support is required for severe intoxication. Standard management of poison ingestion, including

superactivated charcoal, should be used following oral ingestion.

c. Prognosis. Prognosis following an aerosol challenge is poor.

4-36. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in patient care. Saxitoxin is not transmitted person to person.

4-37. Medical Evacuation

Patients may be evacuated. Apply Standard Precautions during evacuation.

Section VI. STAPHYLOCOCCAL ENTEROTOXIN B

4-38. General

a. Etiologic Agent. Staphylococcal enterotoxin B is one of numerous exotoxins produced by

Staphylococcus (S.) aureus. Up to one-half of all clinical isolates of S. aureus produce exotoxins; related

toxins include toxic shock syndrome toxin-1 (TSST-1) and exfoliative toxins. The SEB toxin is heat-stable

and is the second most common source of outbreaks of food poisoning.

b. Reservoir. The reservoir of S. aureus is humans (especially, food handlers with infected cuts

on their hands, abscesses, acne eruptions, nasal discharges, or on occasion, from normal appearing skin)

and contaminated milk or milk products. The SEB is usually produced in foods contaminated with S. aureus.
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c. Transmission. Ingestion of food, milk, or milk products containing preformed toxin.

d. Endemic Disease. Staphylococcal food poisoning features the acute onset of fever, nausea,

vomiting, and diarrhea within hours of intoxication. The toxin increases intestinal peristalsis; severe nausea

and vomiting may be due to stimulation of the CNS. The staphylococcal enterotoxins belong to a class of

potent immune stimulants known as bacterial superantigens. Superantigens bind to monocytes at major

histocompatibility complex type II receptors rather than the usual antigen binding receptors. This leads to

the direct stimulation of large populations of T-helper cells while bypassing the usual antigen processing and

presentation. This results in a brisk cascade of pro-inflammatory cytokines and recruitment of other

immune effector cells, and a relatively deficient activation of counter-regulatory negative feedback loops.

This results in an intense inflammatory response that can injure host tissues.

4-39. Biological Warfare Agent Delivery

The primary threat is SEB aerosol release. The SEB may also be employed by sabotage contamination of

food and/or water supplies.

4-40. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory identification. Preventive

medicine/PHS/BEE personnel collect suspect contaminated water samples for laboratory identification.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples. Veterinary personnel

collect specimens from government-owned animals for supporting laboratory identification. Medical

treatment personnel collect specimens from patients presenting with signs and symptoms for laboratory

identification. The supporting laboratory performs toxin assay of epidemiologically implicated food or

water. The laboratory can also perform toxin assay of environmental samples following an aerosol attack.

4-41. Prevention

a. Pre-exposure Prophylaxis. Currently, there is no pre-exposure prophylaxis available.

Protecting food and water supplies from contamination and avoiding potentially contaminated food and

water will protect individuals from the effects of ingested toxins.

b. Post-exposure Prophylaxis. Currently post-exposure prophylaxis is not available; however,

passive immunization (immunoglobulin) can attenuate experimental disease in experimental animals if given

within 4 to 8 hours post-exposure. There are no human data or practice guidelines.

4-42. Biological Warfare Clinical Presentation

a. Incubation. Variable. 4 to 10 hours for GI illness.
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b. Signs and Symptoms. Illness due to poisoning of food or water supplies will present as acute

GI illness (see endemic disease, paragraph 4-38). Illness due to inhalation will result in respiratory tract

disease not encountered in the endemic disease. This is due to the activation of pro-inflammatory

cytochylema cascades in the lungs, leading to pulmonary capillary leak and pulmonary edema. Symptoms

include fever, headache, myalgia, nonproductive cough, and in severe cases, dyspnea. Gastrointestinal

symptoms may also occur due to inadvertent swallowing of SEB delivered via aerosol and deposited in the

upper aero-digestive tract, or coughed following mucociliary clearance. Severe cases may result in acute

pulmonary edema and respiratory failure.

4-43. Diagnosis

Diagnosis includes performing toxin assay (antigen detection) of implicated food or water and on

environmental samples collected following a suspect BW attack. Clinical specimens that could be sent for

toxin assay include serum and respiratory secretions. However, the toxin may not be detectable before the

onset of symptoms. Acute and convalescent sera for antibody tests will confirm the diagnosis. Nonspecific

findings may include leukocytosis, elevated sedimentation rate, and in severe cases, chest x-ray abnormalities

featuring pulmonary edema. Differential diagnosis include pneumonia due to viruses, mycoplasmas,

Chlamydia pneumoniae, Coxiella burnetii, Hantavirus pulmonary syndrome, CW agent inhalation injury (mustard,

phosgene), and in severe cases, other diverse causes of noncardiogenic pulmonary edema and ARDS.

4-44. Treatment

a. Triage Categories. Triage categories will vary with conditions and available resources.

Patients with acute respiratory distress should be placed in the Immediate category to obtain respiratory

support. Patients without respiratory distress should be placed in the Delayed category.

b. Medical Management. Medical management is primarily supportive care; symptomatic relief

may be provided by the use of acetaminophen and cough suppressants. Severe cases will require intensive

care including respiratory support, hemodynamic monitoring, and possibly diuretics and vasopressors.

c. Prognosis. Staphylococcal enterotoxin B is considered an incapacitating agent; most patients

may be expected to make a full recovery, although most patients will be unfit for duty for 1 to 2 weeks.

Patients with pulmonary edema and respiratory failure will be at risk for mortality.

4-45. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in patient care. Staphylococcal enterotoxin B is not communicable person to person.

4-46. Medical Evacuation

Patients may be evacuated. Observe Standard Precautions in patient movement.
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Section VII. TRICHOTHECENE MYCOTOXINS

4-47. General

a. Etiologic Agent. Trichothecene (T2) mycotoxins are a diverse group of over 40 compounds

produced by molds of the genus Fusarium. These toxins inhibit protein and DNA synthesis, mitochondrial

respiration, and alter cell membrane structure and function. Naturally occurring mycotoxicosis occurs in

livestock following ingestion of grains contaminated with molds.

b. Reservoir. Moldy grain.

c. Transmission. Ingestion of moldy grains.

d. Endemic Disease. While there have been no laboratory-confirmed cases of human disease due

to T2 mycotoxins, these toxins are thought to have caused an epidemic of foodborne illness (alimentary

toxic aleukia) in Russia during World War II due to the ingestion of foods prepared from moldy grain.

4-48. Biological Warfare Agent Delivery

The toxin may be delivered by aerosol release or through contamination of food and water supplies. These

toxins are the agents allegedly delivered via aerosol during the Yellow Rain attacks in Afghanistan and

Southeast Asia during the 1970s and 1980s. The T2 mycotoxins are the only potential BW agents that can

harm and be absorbed through intact skin.

4-49. Environmental Detection

The NBC reconnaissance teams collect aerosol samples for supporting laboratory identification. Preventive

medicine/PHS/BEE personnel collect suspect contaminated water samples for laboratory identification.

Veterinary/PVNTMED/PHS personnel collect suspect contaminated food samples. Veterinary personnel

collect specimens from government-owned animals for supporting laboratory identification. Medical

treatment personnel collect specimens from patients presenting with signs and symptoms for laboratory

identification. The supporting laboratory performs toxin assay of epidemiologically implicated food or

water. The laboratory can also perform gas-liquid and high-pressure liquid chromatography of

environmental samples.

4-50. Prevention

a. Pre-exposure Prophylaxis. As a pre-exposure prophylaxis, the use of topical antivesicant

cream or ointment may provide limited protection of skin surfaces. Food and water contaminated with

mycotoxins must not be consumed.

b. Post-exposure Prophylaxis. There is no post-exposure prophylaxis.
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4-51. Biological Warfare Clinical Presentation

a. Incubation. The incubation period is minutes after exposure.

b. Signs and Symptoms. The BW disease presentation will vary according to the portal of entry

and delivered dose. Mycotoxins are highly cytotoxic and may be viewed as radiomimetic agents, or

having effects similar to vesicants, especially mustard agents. Delivery to the skin may cause a burning skin

pain, redness, tenderness, blistering, and progression to skin necrosis with eschar formation and sloughing.

Respiratory exposure may result in nasal itching with pain, rhinorrhea, sneezing, epistaxis, dyspnea,

wheezing, and cough. Exposure of the conjunctivae and other mucosal surfaces may result in local burning

pain and redness, followed by necrosis. Gastrointestinal exposure would be expected to result in nausea,

vomiting, crampy abdominal pain, and watery or bloody diarrhea. Systemic absorption may follow

delivery via any route and would result in late toxicity of decreased blood cell counts, predisposing to

bleeding and sepsis.

4-52. Diagnosis

Serum and urine should be sent for antigen detection. The parent toxin and metabolites (50 to 75 percent)

are eliminated in urine and feces within 24 hours; however, metabolites can be detected as late as 28 days

after exposure.

4-53. Treatment

a. Triage Categories. The triage category varies with the stage and severity of illness and

available resources.

b. Medical Management. Following oral ingestion, standard therapy for poison ingestion

including the use of superactivated charcoal is indicated. Other measures of supportive care depend upon

the organ system involved (for examples, respiratory support for respiratory involvement and standard burn

care for cutaneous involvement). All medical interventions are supportive; there are no antidotes or other

specific therapies available.

c. Prognosis. Prognosis following the development of symptoms is poor.

4-54. Control of Patients, Contacts, and Treatment Areas

Apply Standard Precautions in patient care. Mycotoxins are not transmitted person to person.

4-55. Medical Evacuation

Patients may be evacuated. Observe Standard Precautions during evacuation.
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

APPENDIX A

RECOGNITION OF A

BIOLOGICAL WARFARE AGENT CASUALTY

A-1. General

a. Medical personnel must be familiar with the signs and symptoms of BW agent casualties.

With current technology, it is likely that a BW attack will be completed before the local commander, or his

medical advisor, is aware that it has taken place. The medical officer must attempt to distinguish between

an epidemic of natural origin and a BW attack.

b. Medical and tactical intelligence channels should communicate with each other as early as

possible. Threat information on potential enemy force use of BW weapons/agents is important for planning

and executing HSS operations. Once BW agents have been used, identification of agents will be important

to medical intelligence channels for operational purposes.

c. Medical units should rely on information not only from detectors and intelligence sources, but

also from the casualties themselves. This applies particularly to BW weapons/agents since at present there

are no rapid methods of detection or identification. Some of the problems in the recognition and diagnosis

of casualties suffering from the effects of BW operations are discussed here. Medical personnel must

remember that the signs and symptoms of most BW agents are identical to or similar to those of endemic

and epidemic diseases. The nature and timing of symptoms will vary with the route of exposure. Although

most BW agents require days to manifest, some agents produce their effects in minutes to a few hours. It is

important that the fullest and earliest information be given to medical units when the enemy has used BW

weapons/agents. This information is used to facilitate the diagnosis of individual cases, to initiate immediate

treatment, and to permit the arrangement for the reception of casualties.

A-2. Types of Casualties

On the BW battlefield, the following types of casualties may be seen:

a. Conventional Casualties.

(1) Conventional casualties with no BW injury and with no contamination of their clothing

and equipment.

(2) Conventional casualties with no BW injury but with contamination of their clothing and

equipment.

b. Direct Biological Warfare Casualties.

(1) Biological warfare agent casualties with no other injury.

(2) Mixed casualties with conventional and BW injuries. Since BW munitions often include

burst charges, such injuries may occur as part of a BW agent attack. They may also be present when the
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

BW injury and conventional injury occur at different times. Other types of mixed casualties may be from

nuclear or chemical weapons used as well as the biological weapons. Also, mixed casualties may result

when biological injuries are combined with natural illnesses (infectious disease still accounts for the majority

of casualties in conventional warfare).

c. Indirect Biological Warfare Casualties.

(1) Casualties suffering combat stress reaction occur often in warfare, but may be more

frequent where NBC threats exist. The service member will have the additional stress of isolation from

wearing the chemical protective ensemble; additional fatigue when wearing the protective garments; and

fear of NBC agents. See FM 8-51, FM 22-51, and MCRP 6-11c for additional information on combat

stress control.

(2) Some BW agent treatments can have undesirable side effects when taken inappropriately,

or in large enough quantities. Antibiotics kill desirable bacteria in the digestive tract, causing abdominal

pain and frequent bowel movements. Medical personnel must be alert for their appearance.

(3) Wearing the protective ensemble makes dissipation of excess body heat more difficult.

Wearing the mask also makes water intake difficult. Both will increase the probability of heat injury (heat

exhaustion or heat stroke).

(4) Indirect BW casualties will most likely be the largest group requiring treatment.

A-3. Recognize Biological Casualties

a. It is unlikely that BW agents will produce single casualties under field conditions. Also, a BW

attack should be suspected with any sudden increase in the numbers of unexplained casualties presenting

with the same signs and symptoms. If BW operations are unlikely, and if relatively few service members

are affected, an endemic or epidemic disease may be more probable (for example, Salmonella food

poisoning). If the number of cases continue to present over an extended period, as opposed to a large

number presenting in one or two days, a naturally occurring epidemic is suspected.

b. Under operational conditions, the psychological effects may complicate the medical situation.

To determine if a BW agent has caused the casualty, the medical officer should ask questions along the

following lines:

 Was the casualty wearing full MOPP at the time of the exposure?

 Was there any aircraft or artillery bombardment in the area at the time of the attack?

 Was there anyone in the area dispersing a suspicious spray or vapor from portable or

vehicle-mounted devices?

 Were there any suspicious persons around the unit water supply or in the unit food

service area?
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

 Was there any evidence of spray, liquid droplets, or suspicious persons in the area?

 Was anyone else affected and if so, what effects?

c. To recognize a BW attack, the identity of the agent must be determined.

(1) The medical officer should consider the following:

 Groups of patients from a specific unit/area presenting with the same illness signs

and symptoms in a short period of time (hours to days).

 Signs and symptoms not associated with any known endemic diseases in the AO.

(2) Also, question the patient about the delay or rapidity of the onset of symptoms. Was

there any delay between exposure or contamination and the onset of effects? If so, how long was the delay?

 Did the effects persist after adjustment of the protective mask?

 Has the casualty used any self-injection device or did anyone else use any injection

devices on the casualty? If so, did the symptoms improve or deteriorate?

 Is the casualtys behavior normal?

d. To assess the dose of the agent received by the patient, determine the following:

 Was the casualty exercising or at rest?

 Was the casualty in the open or under cover?

 How long was the suspect BW agent inhaled?

 How long was the interval between suspected contamination and decontamination?
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

APPENDIX B

MEDICAL MANAGEMENT AND TREATMENT

IN BIOLOGICAL WARFARE OPERATIONS

Section I. US ARMY MEDICAL TREATMENT FACILITIES

B-1. General

All US Army MTFs must be prepared to receive mass casualties caused by exposure to BW agents. A mass

casualty situation exists when the number and type of casualties exceed the local medical support capabilities

for their care. If the unit follows conventional operational standing operating procedures, an overwhelming

backlog of work will rapidly accumulate. Such backlogs can result in unnecessary loss of life and limb with

suffering. Therefore, all HSS planners must prepare plans for mass casualty situations and all units must be

trained and equipped for these plans. The unit must be ready to operate with minimal confusion. Medical

units must provide medical treatment to these casualties and supervise their decontamination. Normally,

individual service members are responsible for their own decontamination. For casualties who are injured

and unable to decontaminate themselves, this process has to be performed by buddy aid, by unit personnel

at a decontamination site, or at an MTF by nonmedical personnel from the supported units.

a. At US Army Levels I and II (unit, division, and nondivisional) units, the supported unit

commander must provide at least 8 nonmedical personnel to perform patient decontamination. At US Army

Levels III and IV (corps and echelons above corps) hospitals, a 20-man patient decontamination augmentation

team or 20 nonmedical personnel must be provided to perform patient decontamination. The base cluster

commander or units within the geographical area of the hospital must provide the 20 nonmedical personnel.

b. Medical personnel must supervise patient decontamination personnel to ensure patient

conditions are not aggravated by decontamination process. Supervising medical personnel must make the

final determination on the completeness of patient decontamination.

c. If the supported units do not have the necessary resources to provide nonmedical personnel,

the units (not the medical services) must address this issue with higher headquarters.

B-2. Objectives of Health Service Support in Biological Warfare Operations

The objectives of HSS in BW operations are to

a. Return to duty the maximum number of personnel as soon as possible.

b. Manage casualties so that BW agent injuries are minimized and any other injuries or illnesses

are not aggravated.

c. Protect persons handling contaminated casualties or working in contaminated areas.

d. Avoid spreading contamination in ambulances, other evacuation vehicles and aircraft, MTFs,

and adjoining areas.
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

e. Continue the MTFs operations to maintain normal services unrelated to the medical treatment

of BW agent illnesses and injuries.

B-3. Planning for the Management and Treatment of Biologically Contaminated Casualties

The initial management and treatment of casualties contaminated with a BW agent will vary with the tactical

situation and the nature of the contaminant. Therefore, each MTF must have a plan and put it into effect

immediately, then modify it to meet each specific situation. Patient decontamination sites are collocated

with an MTF. This ensures that medical supervision of patient decontamination is available. Specifics on

management of BW-contaminated patients at the MTF are found in FM 8-10-7. Each MTF has identical

medical equipment sets (MES) for chemical agent patient decontamination and treatment. The numbers of

each type of MES vary, depending on the level of care. For example, the battalion aid station (BAS) has

one chemical agent patient decontamination MES and two chemical agent patient treatment MES. The

patient decontamination MES provides sufficient supplies to decontaminate 60 patients. Each chemical

agent patient treatment MES provides sufficient medical supplies to treat 30 patients. The chemical agent

patient treatment MES contains the patient protective wraps (PPWs) that are needed to transport

decontaminated litter patients to the next level MTF. Each MTF must be prepared to treat

 Biological warfare agent casualties generated within the geographical area of the MTF.

 Patients received from a forward and, in some cases, a lateral MTF.

 Patients suffering from a combination of injuries/illnesses (such as BW and conventional, BW

and chemical agent, and BW and endemic disease.)

 Patient suffering from battle injuries and DNBIs that have not been exposed to any NBC agents.

 Enemy prisoners of war, detained persons, and noncombatants, when directed.

B-4. Emergency Medical Treatment of Biologically Contaminated Casualties

a. Biological warfare agent casualties received at an MTF may also have traumatic wounds or

illnesses due to other causes. Management of these patients must minimize the BW agent injuries without

aggravating their traumatic wounds or illnesses.

b. Triage of arriving casualties is extremely important. A decision is made whether EMT or

decontamination of the casualty requires priority. Airway management and/or control of hemorrhage may

be equal to or more urgent than treatment for BW agent poisoning. Therefore, EMT measures may have to

be performed in rapid sequence with decontamination or by simultaneous team actions.

c. For contaminated casualties who have traumatic injuries or other illnesses, decontamination

should be accomplished as soon as the situation permits. Lifesaving measures for a traumatic injury or

some illnesses must be given priority over immediate decontamination, although the delay may increase the

BW agent illness or injury.
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

d. When a contaminated casualty has another injury or illness resulting in respiratory difficulty,

hemorrhage, or shock, the order of priority for emergency action is as follows:

(1) Control respiratory failure (provide assisted ventilation) and/or massive hemorrhage.

(2) Decontaminate the casualty.

(3) Administer additional EMT for shock, wounds, and illnesses so severe that delay may be

life or limb threatening.

(4) Evacuate the casualty as soon as possible, if necessary.

B-5. Patient Decontamination Methods

a. Patient decontamination serves two purposes

(1) It prevents the patients system from absorbing additional contaminants.

(2) It also protects medical personnel treating the patient and other patients from

contamination. Accumulated contamination in the MTF is a serious threat to medical personnel and

patients. Accumulated contamination may also impose a serious medical logistical burden on the unit. The

effectiveness of decontamination is strongly influenced by the time lapse between initial contamination and

decontamination. In many cases, the patient may have absorbed dangerous quantities of a contaminant

before arriving at the MTF.

b. Each service member is trained in immediate decontamination procedures and is equipped to

do so. However, any patient arriving at an MTF from a BW-contaminated area is considered contaminated,

unless there is positive proof to the contrary.

c. A decontamination area is established on the downwind side of the MTF. It is provided with

overhead protection such as plastic sheeting, trailer covers, ponchos, tarpaulins, or tents. Only those

patients requiring treatment at a forward MTF will have their protective overgarments and other clothing

removed. Needless removal of protective clothing only increases the patients vulnerability to liquid agent

exposure which results in increased injury. Also, forward MTFs do not have replacement protective

overgarments. Any ambulatory patient decontaminated by clothing removal becomes a litter patient; he

must be placed in a PPW for protection from BW agents during evacuation. Patients not requiring

treatment at a forward MTF, but requiring evacuation to the next level MTF must have their MOPP gear

and equipment spot decontaminated. Spot decontamination will remove gross contamination, reducing the

hazard to the casualty and evacuation personnel.

d. Every person entering the decontamination area (including patients) must be wearing a

protective mask or have other respiratory tract protection in place. Most contaminants are removed by

carefully removing all clothing.
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

WARNING

Do not remove the patients protective mask. Remove the

mask hood, overgarments, booties and boots, the BDU, and

undergarments. For step-by-step procedures in performing

patient decontamination, see FM 8-10-7.

e. After patients have been decontaminated, exercise rigid control to prevent exposing their

unprotected skin to a liquid BW agent. After treatment in the clean treatment area or collective protection

shelter (CPS), the patient is placed in a PPW (to protect them during evacuation) and taken to the evacuation

point to await evacuation. Medical personnel must monitor patients at the evacuation point to ensure that

their condition remains stable; if their condition changes, additional treatment may have to be provided

before evacuation.

f. Ambulatory patients may be able to decontaminate themselves and assist with the

decontamination of other ambulatory patients. Their overgarments are not removed unless they must enter

the clean treatment area or CPS for treatment. For patients not entering the clean treatment area or CPS,

spot decontaminate the overgarment to remove gross contamination. When possible, have them proceed as

groups of two or three to facilitate control. Ambulatory patients require constant observation and periodic

assistance during the decontamination process. The aidman at the decontamination point removes all

bandages from patients that will be treated at the MTF. Bandages are not replaced unless needed to control

bleeding. After decontamination, each patient goes through the shuffle pit to the clean treatment area where

wounds are treated and if possible, protective covering is restored. Restore protective covering by taping

holes or tears in the protective overgarment. Patients are then returned to duty or go to the evacuation

point, as their medical conditions dictate. Ambulatory patients with injuries that do not require immediate

attention but require treatment at a higher level MTF are evacuated in their MOPP ensemble. For example,

a patient with a broken arm has a stabilizing splint on. This individual does not require treatment at the

BAS; however, his MOPP gear must be spot decontaminated to remove gross contamination before

evacuation to the Level II MTF.

NOTE

At forward MTFs (Levels I and II), only patients that cannot survive

evacuation to the next level MTF will be completely decontaminated

(have their clothing removed) and treated at the lower level of care

facility. Patients that are stable but require evacuation to a higher

level MTF should have their overgarments spot decontaminated before

evacuation. The patients must be completely decontaminated at the

MTF where essential medical care is provided.
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

B-6. Logistics

a. Provisions must be made to ensure that medical personnel are supplied and equipped to

manage and treat contaminated casualties. Also, supplies and equipment must be provided for the protection

of personnel manning the contaminated areas. Medical supplies are stored or stocked in a manner that

reduces potential loss from BW contamination.

b. Patient protective wraps must be available for casualties whose injuries require decontamination

(clothing removal) for treatment in the clean treatment area. After treatment, decontaminated patients must

be placed in PPWs before they are moved to the evacuation point (paragraph B-5e above).

B-7. Training

Commanders must ensure that medical personnel and decontamination team members (provided by the

supported unit) are trained to manage, decontaminate, and treat BW agent casualties. Personnel must be

trained to protect themselves from BW agent injuries. In addition, provisions must be made for practice

exercises to enable them to accomplish their responsibilities with speed and accuracy. Example:

Decontaminating a casualty with speed is achieved through practice. Training emphasis should be placed on

 Employing individual protection.

 Practicing immediate decontamination procedures.

 Providing EMT.

 Performing casualty decontamination.

 Evacuating decontaminated casualties.

 Evacuating contaminated casualties.

 Sorting and receiving contaminated casualties into a system designed for the treatment of both

contaminated and uncontaminated casualties.

 Techniques for patient lifting and litter transfer.

 Using the chemical agent monitor (CAM) and chemical agent detection paper to monitor for

and detect chemical agents, if employment in conjunction with BW agents is suspected.

B-8. Casualty Evacuation

a. Contaminated casualties should be decontaminated as close to the areas where they were

contaminated as possible. Their MOPP gear and clothing should not be removed until they arrive at an MTF.

Evacuation by ground ambulance must not be delayed for completion of decontamination. Upon arrival at

the MTF where treatment will be provided, all contaminated clothing and equipment (except the protective
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FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

mask) are removed and the skin and protective mask are decontaminated; spot decontaminate the skin.

Decontaminated patients continue to be a hazard to persons handling, treating, or transporting them.

Therefore, appropriate precautions for the suspected disease must be applied. After decontamination at the

field MTF, the patient is placed in the clean holding area to await admission into the CPS or clean treatment

area. They must be protected from recontamination. Patients will keep their protective mask on until they

are in the clean treatment area (away from the hotline) or are in the air lock of the CPS (see FM 8-10-7).

(1) Once treated, the patient is placed in a PPW before movement to the evacuation pickup

point. The PPW protects the individual from further contamination. Individuals inside the PPW no longer

have to wear the protective mask and are evacuated as clean. A plastic window in the PPW permits patient

observation. A patient in a PPW and left in a sunny area is subject to heat build up. The protective mask

remains with the patient during evacuation even though it may not be worn.

(2) If a BW attack occurs, medical units in the evacuation system can expect to receive

contaminated casualties because of the need for hasty evacuation. Therefore, extreme care must be taken to

avoid spreading the contamination.

b. Before contaminated casualties are evacuated by Army aircraft or landing craft, they should be

decontaminated. Otherwise, the BW agent may endanger the crew and other personnel, as ventilation is

poor in aircraft compartments and other enclosed spaces. If casualties cannot be decontaminated before

evacuation, they should be evacuated by ground ambulance. These casualties should wear their protective

masks. The hazards of the BW agent to other persons can be further minimized by

 Preparing each litter by placing an impermeable cover over it and an open blanket on top

of the cover.

 Placing the casualties on the prepared litters and folding the sides of the blankets over

them. Although this measure helps protect other persons, it increases the casualties exposure to the

contaminant and increases the possibility of heat injuries.

 Providing as much ventilation during transport as the weather and other conditions permit.

 Removing the impermeable covers and blankets with the casualties when they are

removed from the vehicles. Litters that have not been protected with impermeable covers must be handled

as contaminated.

c. Patients being evacuated by USAF AE aircraft should be decontaminated prior to evacuation.

See FM 8-10-6 and FM 8-10-7 for procedures on patient evacuation by USAF aircraft.

Section II. US AIR FORCE MEDICAL TREATMENT FACILITIES

B-9. General

a. The USAF recognizes five levels of care.
B-7

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

(1) Level I includes self-aid and buddy care, examination and emergency lifesaving measures

such as maintenance of airway, control of bleeding, prevention and control of shock, and prevention of

further injury. Medical treatment is administered by independent duty medical personnel.

(2) Level II care is administered at the Air Transportable Clinic which assumes AE

availability. Patients are stabilized for AE. There is limited outpatient clinical services, initial trauma

response, and no patient holding capability.

(3) Level III care is provided by the Air Transportable Hospital (ATH). There are 10-bed,

25-bed, and 50-bed ATH packages. Normally, individual service members who were exposed to a BW

agent and are in need of medical care are assisted by the WMDT in the decontamination process. For

casualties who are injured and unable to decontaminate themselves, this process has to be performed by the

WMDT. (Public health technicians on the WMDTs also have a secondary mission to provide technical

guidance on food decontamination.)

(4) Level IV care provides definitive therapy for patients in the recovery phase. If rehabilitation cannot be accomplished within a pre-determined holding period, patients are evacuated to Level V.

(5) Level V care is convalescent, restorative, and rehabilitative. Level V care is normally

provided by military, Department of Veterans Affairs, or civilian hospitals in CONUS.

b. Military personnel exposed to sufficient BW agents without personal protective equipment and

without immunity or prophylaxis will become medical casualties when 75 percent incapacitated.

Commanders must be aware that military personnel who become BW medical casualties will require

medical treatment for more than 7 days and it is unlikely that they will be recovered to 75 percent capacity

to permit return to duty until after a lengthy convalescent period. In-theater commanders must make

arrangements for medical evacuation of BW casualties and arrangement for replacement personnel.

Continental US commanders must prepare for at least a 10-day forecast of patient loads from theater

commanders and identify resources for treatment and recovery of BW patients. Special resources and

transportation requirements will be required for casualties exposed to IQDs; see paragraph 1-21.

B-10. Detection of Biological Agents

a. For information on the employment, physical properties, infectivity, detection, and control of

biological agents, see AFJMAN 32-4009 and AFVA 32-4011. Basically, protection consists of denying

access of the agent to the respiratory and digestive systems and immunization of individuals. Skin and

wound contamination is of secondary importance.

b. If a real-time field detection/identification capability is not present, recognition of BW agents

must be based on epidemiology and symptoms. Once illness begins to appear, the presence of an airborne

BW agent should be relatively obvious because of the large numbers of casualties and the absence of a

common exposure source such as food or water. However, food and/or water may also serve as a vehicle

of transmission. If the situation is not readily apparent, the attack will not have been effective. Some

indications of an attack are
B-8

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

 Point-source epidemiology with a record number of sick and dying patients presenting

within a short period of time (within 12 to 48 hours).

 Very high attack rates (60 to 90 percent of personnel are affected/symptomatic).

 A high incidence of pulmonary involvement signaling an aerosol route of infection. This

would apply to such agents as plague, tularemia, anthrax, and Q fever where the usual form of infection is

not pulmonary.

 Impossible epidemiology. If CCVHF occurred in Alaska or New York, or VEE in

England, a man-made epidemic would be extremely likely.

 Record fatality rates would be expected for many agents, since a large number of victims

would receive doses of organisms far beyond what could possibly occur in nature. This is especially true of

an aerosol attack.

 Localized areas of disease epidemics might occur in an area or sector downwind from the

point of attack.

 Multiple infections at a single site with unusual pathogens.

 Increased numbers of dead animals of all species, such as rats for plague, or horses with

equine encephalitis viruses.

 Protection of those working in indoor environments or environments with filtered air at

the time of the attack.

 The near simultaneous outbreak of similar or different epidemics at the same site or at

different sites in a TO or at military installations around the world.

 Direct evidence of an attack, such as finding an unexploded munitions or a contaminated

exploded munitions; admission by hostile forces or terrorists that BW weapons are being used; witnessing

an attack; or intelligence information reporting use of BW agents by hostile forces from covert agents

working within those hostile forces.

B-11. Identification

The MTF should attempt to identify the agent using whatever laboratory resources are available. The MTF

should collect and transport appropriate environmental samples and biological specimens to more capable

medical laboratory facilities, such as the Forward Naval Laboratory or the Area Medical Laboratory.

B-12. Decontamination

Normally, only life-saving medical treatment can be provided prior to decontamination, as described in

AFJMAN 44-149. Decontamination of casualties is normally done by the 19-member WMDT (Unit Type
B-9

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Code [UTC] FFGLB) using the equipment package UTC FFGLA. Decontamination is performed prior to

the delivery of definitive care in MTFs. Supplies are sufficient to perform complete body skin

decontamination of 500 casualties, but should be reviewed and modified to support local wartime tasking

and types of decontamination (DECON) facilities. For example the DECON facility can be connected to

the chemically hardened ATH via air locks at one end of the emergency room/triage area. Decontamination

is performed to arrest the action of the contaminant on the patient and prevent further contamination of

patients, medical personnel (who may work without protective equipment to maintain full patient care

capabilities) and medical assets. Decontamination does not imply absolute removal of contaminants. The

outer layer of clothing is removed and contaminated skin is washed with germicidal soap or 0.5 percent

hypochlorite and warm water. The clothing removal step in the decontamination process offers the greatest

opportunity for contaminant removal. Removal of the BDO normally decontaminates approximately 90 to

94 percent of the BW agent. If removal of the BDO adequately decontaminates the patient, the rest of the

clothing is not removed. Masks are not removed from patients until they have been transferred out of the

liquid and vapor hazard areas. Exception: The mask can be removed from the patient for emergency

airway management or resuscitation by the EMT trained personnel assigned to the WMDT. The resuscitation

device, individual chemical (RDIC) must be used to prevent exposing the patient to secondary aerosolization

hazards. (See FM 8-10-7 and USAF WMDT CONOPS for complete details on patient decontamination.)

Section III. US NAVY MEDICAL TREATMENT FACILITIES

B-13. General

For purposes of this publication, US Navy Level I MTFs include battle dressing stations and medical

departments of US naval vessels, and BASs in support of the Fleet Marine Forces, regardless of the

presence of a physician. Where this manual differs from Navy and Marine Corps doctrine, such doctrine

shall have precedence.

a. Although the decontamination of naval personnel is considered a nonmedical function, it is

accepted that the potential scenario exists in which contaminated personnel might arrive at an MTF.

Therefore, all arriving casualties should be considered contaminated until proven otherwise, and all levels

should be prepared to receive such casualties.

b. Because of the variation in supported units, readers are referred to unit and higher level

medical policy in determining assignment of necessary decontamination personnel.

c. No casualty will be denied medical treatment to the degree necessary, given overall medical

condition, local resources, other casualty demands, availability of evacuation, and proximity to higher

levels of care, solely due to casualty contamination. This is not to be construed, however, as to preclude

triaging a contaminated patient to the Expectant category. Such Expectant category patients should still be

provided minimal care, comfort, pain relief, and other measures as available.
	





				



	

		


 	

	
	




 





 



	

 





 


 
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C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

EMT emergency medical treatment

 EO Executive Order

F. Francisella

F Fahrenheit

FDA Food and Drug Administration

FM field manual

GI gastrointestinal

gm gram(s)

GU genitourinary

HEPA high efficiency particulate air

HFRS hemorrhagic fever with renal syndrome

HIV human immunodeficiency virus

HSS health service support

IATA International Air Transportation Association

IgG immunoglobulin class G

IgM immunoglobulin class M

IM intramuscular(ly)

IND investigational new drug

IQD internationally quarantinable disease

IV intravenous

JBPDS Joint Biological Point Detection System

JPO-BIO Joint Program Office for Biological Defense

JSLIST Joint service lightweight integrated suit technology

kg kilogram(s)
Glossary-4

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

km kilometer(s)

LRBSDS Long-Range Biological Standoff Detection System

MCRP Marine Corps Reference Publication

MES medical equipment sets

mg milligram(s)

ml milliliter(s)

MOPP mission-oriented protective posture

MRI magnetic resonance imaging

MTF medical treatment facility

NATO North Atlantic Treaty Organization

NAVMED P US Navy Medical Publication

NBC nuclear, biological, and chemical

PCR polymerase chain reaction

PHS public health service

PPW patient protective wrap

PSP paralytic shellfish poisoning

PVNTMED preventive medicine

Q fever Query fever

QSTAG Quadripartite Standardization Agreement

RDIC resuscitation device, individual chemical

RNA ribonucleic acid

S. Staphylococcus

S2 Intelligence Officer (US Army)






				

 
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C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

epizootic A disease that is only present in an animal population for limited periods, but has a high

morbidity rate.

etiologic Cause of the disease/illness.

inoculum The amount of microorganisms introduced into a host.

 off-label indication The use of licensed medications for purposes that are not approved by the FDA. Offlabel usage is common practice in general medical care.

passive immunization The administration of pre-formed antibodies to confer immunity to a specific

pathogen or toxin.

sample Material collected from a source other than an animal or man for laboratory analysis (such as

water sample or soil sample).

specimen Material collected from a man or animal for laboratory analysis (such as tissue or blood

specimen).

Standard Precautions Handwashing after patient contact. Using gloves when touching blood, body

fluids, secretions, excretions, and contaminated items. Using mask, eye protection, and gown during

procedures likely to generate splashes or sprays of blood, body fluids, secretions, or excretions. Handling

contaminated patient-care equipment and linens in a manner that prevents the transfer of microorganisms to

people or equipment. Practicing care when handling sharps and using a mouthpiece or other ventilation

device as an alternative to mouth-to-mouth resuscitation, when practical. Placing the patient in a private

room if they contaminate the environment, when feasible.

toxin agents Poisonous by-products of living organisms used to cause disease, illness or death in susceptible

individuals.

viral agents A group of viruses that have been selected as BW agents because of their ability to produce

disease, illness, and death in susceptible individuals.
References-1

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

REFERENCES

 Executive Order

13139. Improving Health Protection of Military Personnel Participating in Particular Military Operations. 30 September 1999.

Joint Publications

Joint Pub 4-02. Doctrine for Health Service Support in Joint Operations. 26 April 1995.

Joint Pub 4-02.2. Joint Tactics, Techniques, and Procedures for Patient Movement in Joint Operations.

30 December 1996.

NATO STANAGs

2002. Marking of Contaminated or Dangerous Land Areas, Complete Equipments, Supplies and Stores

(NBC). 6th Edition. 7 November 1978.

2103. Chemical Hazard Prediction. 5th Edition. 1 July 1983.

2104. First Aid and Hygiene Training in NBC Operations. 2d Edition. 10 November 1989.

QSTAG

187. Reporting Nuclear Detonations, Biological and Chemical Attacks, and Predicting and Warning of Associated Hazards and Hazard Areas. 21 May 1998.

Multiservice Publications

FM 3-3. Chemical and Biological Contamination Avoidance. FMFM 11-17. 16 November 1992. (Change 1,

29 September 1994).

FM 3-4. NBC Protection. FMFM 11-9. 29 May 1992. (Change 2, 21 February 1996).

FM 3-5. NBC Decontamination. FMFM 11-10. 17 November 1993.

FM 3-6. Field Behavior of NBC Agents (Including Smoke and Incendiaries). AFM 105-7; FMFM 7-11-H.

3 November 1986.

FM 8-9. NATO Handbook on the Medical Aspects of NBC Defensive Operations. AMedP-6 (B). NAVMED

P-5059; AFJMAN 44-151. 1 February 1996.

FM 8-33. Control of Communicable Diseases Manual. 16th Edition. NAVMED P-5038. 9 April 1996.

US Army Field Manuals

FM 3-101-4. Biological Detection Platoon Operations, Tactics, Techniques, and Procedures. 9 June 1997.

(Change 1, 15 August 1997).

FM 3-101-6. Biological Defense Operations Corps/Company, Tactics, Techniques, and Procedures.

19 March 1999.

FM 8-10-6. Medical Evacuation in a Theater of Operations, Tactics, Techniques, and Procedures.

31 October 1991. (Change 1, 8 March 1994).

FM 8-10-7. Health Service Support in a Nuclear, Biological, and Chemical Environment. 22 April 1993.

(Change 1, 26 November 1996).

FM 8-42. Combat Health Support in Stability Operations and Support Operations. 27 October 1997.

US Air Force Publication

AFVA 32-4011. USAF Standardized Alarm Signals for Areas Subject to NBCC Attack. 1 December 1998.
References-2

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

Civilian Reference Material

Books

Butler, T. Plague and Other Yersinia Infections. New York, NY: Plenum Medical Book Company, 1983.

Eitzen, E., Pavlin, J., Cieslak, T., Christopher, G., Culpepper, R. Medical Management of Biological

Casualties Handbook. 3d Edition. Fort Detrick, Frederick, MD: U.S. Army Medical Research

Institute of Infectious Diseases, 1998.

Fenner, F., Henderson, D.A., Arita, I., Jezek, Z., Ladnyi, I.D. Smallpox and Its Eradication. Geneva,

Switzerland: World Health Organization, 1988.

Fields, B.N., Knipe, D.M., Howley, P.M., et al. Fields Virology. 3d Edition. Philadelphia, PA:

Lippincott-Raven, 1996.

Mandell, G.L., Bennett, J.E., Dolin, R. Principles and Practice of Infectious Diseases. 4th Edition. New

York, NY: Churchill Livingstone, 1995.

Sidell, F.R., Takafuji, E.T., Franz, D.R. Medical Aspects of Chemical and Biological Warfare. (Textbook

of Military Medicine Series, Part I, Warfare, Weaponry, and the Casualty.) Office of The Surgeon

General, Textbook of Military Medicine Publications, Borden Institute, Washington, DC, 1997.

Strickland, Thomas G. Hunter’s Tropical Medicine. 7th Edition. Philadelphia, PA: W.B. Saunders

Company, 1991.

World Health Organization Group of Consultants: Health Aspects of Chemical and Biological Weapons.

Geneva, Switzerland: World Health Organization, 1970.

Journal Articles

Abramova, F.A., Grinberg, L.M., Yampolskaya, O.V., Walker, D.H. Pathology of Inhalational Anthrax

in 42 Cases from the Sverdlovsk Outbreak of 1979. Proceedings of the National Academy of

Sciences, USA (1993), 90:2291-4.

Centers for Disease Control and Prevention. Bioterrorism Alleging Use of Anthrax and Interim Guidelines

for Management-United States, 1998. Morbidity and Mortality Weekly Report (1999), 48:69-74.

Centers for Disease Control and Prevention. Management of Patients with Suspected Viral Hemorrhagic

Fever. Morbidity and Mortality Weekly Report (1988), 37:1-15.

Centers for Disease Control and Prevention. Prevention of Plague. Recommendations of the Advisory

Committee on Immunization Practices (ACIP). Morbidity and Mortality Weekly Report (1996),

45:RR-14 (Suppl).

Centers for Disease Control and Prevention. Update: Management of Patients with Suspected Viral

Hemorrhagic Fever-United States. Morbidity and Mortality Weekly Report (1995), 44:475-9.

Centers for Disease Control and Prevention. Vaccinia (Smallpox) Vaccine: Recommendations of the ACIP.

Morbidity and Mortality Weekly Report (1991), 40:RR-14 (Suppl).

Christopher, G.W., Cieslak, T.J., Pavlin, J.A., Eitzen, E.M. Jr. Biological Warfare: A Historical

Perspective. Journal of American Medical Association (1997), 278:412-417.

Farrar, E.W. Anthrax: Virulence and Vaccines. Annals of Internal Medicine (1994), 121:379-80.

Franz, D.R., Jahrling, P.B., Friedlander, A.M., McClain, D.J., Hoover, D.L., Byrne, W.R., Pavlin,

J.A., Christopher, G.W., Eitzen, E.M. Jr. Clinical Recognition and Management of Patients

Exposed to Biological Warfare Agents. Journal of American Medical Association (1997),

278:399-411.
References-3

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

Friedlander, A.M., Welkos, S.L.L., Pitt, M.L.M., et al. Postexposure Prophylaxis Against Experimental

Inhalation Anthrax. Journal of Infectious Diseases (1993), 167:1239-42.

Garner, J.S. Hospital Infection Control Practices Advisory Committee. Guidelines for Isolation Precautions

in Hospitals. Infection Control Hospital, Epidemiology (1996), 17:53-80, and American Journal of

Infection Control (1996), 24:24-52.

Jackson, P.J., Hugh-Jones, M.E., Adair, D.M., et al. Polymerase Chain Reaction Analysis of Tissue

Samples from the 1979 Sverdlovsk Anthrax Victims: The Presence of Multiple Bacillus Anthracis

Strains in Different Victims. Proceedings of the National Academy of Sciences, USA (1998),

95:1224-9.

McGovern, T.W., Christopher, G.W., Eitzen, E.M. Jr. Cutaneous Manifestations of Biological Warfare

and Related Threat Agents. Arch Dermatol (1999), 135:311-322.

Meselson, M., Guillemin, J.G., Hugh-Jones, M., et al. The Sverdlovsk Anthrax Outbreak of 1979. Science

(1994), 266:1202-1207.

Pile, J.C., Malone, J.D., Eitzen, E.M., Friedlander, A.M. Anthrax as a Potential Biological Warfare

Agent. Archives of Internal Medicine (1998), 158:429-34.

Pomerantsev, A.P., Staritsin, N.A., Mockov, Y.V., Marinin, L.I. Expression of Cereolysine AB Genes in

Bacillus Anthracis Vaccine Strain Ensures Protection Against Experimental Hemolytic Anthrax

Infection. Vaccine (1997), 15:1846-1850.

Turnbull, P.C.B. Anthrax Vaccines: Past, Present, and Future. Vaccine (1991), 533-9.
Index-1

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

INDEX

References are to paragraph numbers except where specified otherwise.

aeromedical isolation team, 1-22

anthrax, 2-2

agent delivery, 2-3

clinical presentation, 2-6

control of patients, contacts, and treatment areas, 2-9

detection, 2-4

diagnosis, 2-7

endemic disease, 2-2d

etiologic agent, 2-2a

evacuation, 2-10

gastrointestinal, 2-6b(2)

immunization, 2-5a(1)

incubation period, 2-6a

inhalation, 2-6b(1)

medical management, 2-8b

oropharyngeal, 2-6b(2)

prevention, 2-5

prognosis, 2-8c

prophylaxis, 2-5

post-exposure, 2-5b

pre-exposure, 2-5a

reservoir, 2-2b

signs and symptoms, 2-6b

transmission, 2-2c

treatment, 2-8

triage, 2-8a

bacterial agent

anthrax, 2-2

brucellosis, 2-11

glanders, 2-29

identification, B-11

melioidosis, 2-20

plague, 2-38

Q fever, 2-47

tularemia, 2-57

biological casualties

recognize, A-1, A-3

types of, A-2

biological warfare agent

casualties

case reporting, 1-14

diagnosis, 1-7

epidemiological assessment, 1-14
Index-2

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

evacuation, 1-21

first aid, 1-17

handling, 1-18

infection control, 1-20

prevention, 1-15

protective measures, 1-18

therapy, 1-13

classification, 1-4

delivery, 1-2, 2-3

detection, 1-6, 2-4

employment, 1-3

identification, 1-12

mode of delivery, 1-2

patient decontamination, 1-19

portal of entry, 1-5

protective equipment, 1-16

specimen

chain of custody, 1-11

collection, 1-8

handling and shipment, 1-10

labeling, 1-9

threat, 1-1

brucellosis, 2-11

agent delivery, 2-12

clinical presentation, 2-15

control of patients, contacts, and treatment areas, 2-18

detection, 2-13

diagnosis, 2-16

endemic disease, 2-11d

etiologic agent, 2-11a

evacuation, 2-19

incubation period, 2-15a

medical management, 2-17b

prevention, 2-14

prognosis, 2-17c

prophylaxis, 2-14

post-exposure, 2-14b

pre-exposure, 2-14a

reservoir, 2-11b

signs and symptoms, 2-15b

transmission, 2-11c

treatment, 2-17

triage, 2-17a

case reporting, 1-14

clostridium botulinum, 4-2
Index-3

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

agent delivery, 4-3

clinical presentation, 4-5

control of patients, contacts, and treatment areas, 4-9

detection, 4-4

diagnosis, 4-7

endemic disease, 4-2d

etiologic agent, 4-2a

evacuation, 4-10

incubation period, 4-5a

medical management, 4-8b

prevention, 4-6

immunization, 4-6a

prognosis, 4-8c

prophylaxis, 4-6

post-exposure, 4-6b

pre-exposure, 4-6a

reservoir, 4-2b

signs and symptoms, 4-5b

transmission, 4-2c

treatment, 4-8

triage, 4-8a

clostridium perfringens, 4-11

agent delivery, 4-12

clinical presentation, 4-15

control of patients, contacts, and treatment areas, 4-18

detection, 4-13

diagnosis, 4-16

endemic disease, 4-11d

etiologic agent, 4-11a

evacuation, 4-19

incubation period, 4-15a

medical management, 4-17b

prevention, 4-14

prognosis, 4-17c

prophylaxis, 4-14

reservoir, 4-11b

signs and symptoms, 4-15b

transmission, 4-11c

treatment, 4-17

triage, 4-17a

decontamination

casualty, 1-19, B-12, B-13

patient, 1-19, B-5, B-13c

WMDT, B-12

emergency medical treatment, B-4
Index-4

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

glanders, 2-29

agent delivery, 2-30

clinical presentation, 2-33

control of patients, contacts, and treatment areas, 2-36

detection, 2-31

diagnosis, 2-34

endemic disease, 2-29d

etiologic agent, 2-29a

evacuation, 2-37

incubation period, 2-33a

medical management, 2-35b

prevention, 2-32

prognosis, 2-35c

prophylaxis, 2-32

reservoir, 2-29b

signs and symptoms, 2-33b

transmission, 2-29c

treatment, 2-35

triage, 2-35a

health service support, B-2

emergency medical treatment, B-4

logistics, B-6

objectives, B-2

planning, B-3

training, B-7

identification of biological agent, B-11

infection control, 1-20

internationally quarantinable disease, 1-21b(3), 2-46, 3-10, B-9b

isolation, 1-20

 investigational new drug, 1-23

laboratory, 1-7

medical

management, B-1

treatment facilities

US Air Force, B-9

US Army, B-1

US Navy, B-13

melioidosis, 2-20

agent delivery, 2-21

clinical presentation, 2-24

control of patients, contacts, and treatment areas, 2-27

detection, 2-22

diagnosis, 2-25

endemic disease, 2-20d

etiologic agent, 2-20a

evacuation, 2-28
Index-5

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

incubation period, 2-24a

medical management, 2-26b

prevention, 2-23

prognosis, 2-26c

prophylaxis, 2-23

reservoir, 2-20b

signs and symptoms, 2-24b

transmission, 2-20c

treatment, 2-26

triage, 2-26a

 off-label indications, 1-23

plague, 2-38

agent delivery, 2-39

clinical presentation, 2-42b

control of patients, contacts, and treatment areas, 2-45

detection, 2-40

diagnosis, 2-43

endemic disease, 2-38d

etiologic agent, 2-38a

evacuation, 2-46

incubation period, 2-42a

medical management, 2-44b

prevention, 2-41

immunization, 2-41b

repellents, 2-41a

prognosis, 2-44c

prophylaxis, 2-41

post-exposure, 2-41d

pre-exposure, 2-41c

reservoir, 2-38b

signs and symptoms, 2-42b

transmission, 2-38c

treatment, 2-44

triage, 2-44a

Q fever

agent delivery, 2-48

clinical presentation, 2-51

control of patients, contacts, and treatment areas, 2-55

decontamination, 2-53

detection, 2-49

diagnosis, 2-52

endemic disease, 2-47d

etiologic agent, 2-47a

evacuation, 2-56

incubation period, 2-51a

medical management, 2-54b
Index-6

C1, FM 8-284/NTRP 4-02.23 (NAVMED P-5042)/AFMAN (I) 44-156/MCRP 4-11.1C

prevention, 2-50

miscellaneous, 2-50a

prognosis, 2-54c

prophylaxis, 2-50

post-exposure, 2-50c

pre-exposure, 2-50b

reservoir, 2-47b

signs and symptoms, 2-51b

transmission, 2-47c

treatment, 2-54

triage, 2-54a

quarantine, 2-46, 3-9

recognize biological casualties, A-1, A-3

type of casualties, A-2

ricin, 4-20

agent delivery, 4-21

clinical presentation, 4-24

control of patients, contacts, and treatment areas, 4-27

detection, 4-22

diagnosis, 4-25

endemic disease, 4-20d

etiologic agent, 4-20a

evacuation, 4-28

incubation period, 4-24a

medical management, 4-26b

prevention, 4-23

prognosis, 4-26c

prophylaxis, 4-23

post-exposure, 4-23b

pre-exposure, 4-23a

reservoir, 4-20b

signs and symptoms, 4-24b

transmission, 4-20c

treatment, 4-26

triage, 4-26a

saxitoxin, 4-29

agent delivery, 4-30

clinical presentation, 4-33

control of patients, contacts, and treatment areas, 4-36

detection, 4-31

diagnosis, 4-34

endemic disease, 4-29d

etiologic agent, 4-29a

evacuation, 4-37

incubation period, 4-33a
Index-7

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

medical management, 4-35b

prevention, 4-32

prognosis, 4-35c

prophylaxis, 4-32

post-exposure, 4-32b

pre-exposure, 4-32a

reservoir, 4-29b

signs and symptoms, 4-33b

transmission, 4-29c

treatment, 4-35

triage, 4-35a

smallpox

agent delivery, 3-3

clinical presentation, 3-6

control of patients, contacts, and treatment areas, 3-9

detection, 3-4

diagnosis, 3-7

endemic disease, 3-2d

etiologic agent, 3-2a

evacuation, 3-10

incubation period, 3-6a

medical management, 3-8b

prevention, 3-5

immunizations, 3-5a, b

prognosis, 3-8c

prophylaxis, 3-5

contraindications, 3-5a

post-exposure, 3-5b

pre-exposure, 3-5a

reservoir, 3-2b

signs and symptoms, 3-6b

transmission, 3-2c

treatment, 3-8

triage, 3-8a

specimen/sample

chain of custody, 1-11

collection, 1-8

handling, 1-10

identification, 1-12

labeling, 1-9

packaging, 1-10

staphylococcal enterotoxin B, 4-38

agent delivery, 4-39

clinical presentation, 4-42

control of patients, contacts, and treatment areas, 4-45
Index-8

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

detection, 4-40

diagnosis, 4-43

endemic disease, 4-38d

etiologic agent, 4-38a

evacuation, 4-46

incubation period, 4-42a

medical management, 4-44b

prevention, 4-41

immunization, 4-41b

prognosis, 4-44c

prophylaxis, 4-41

post-exposure, 4-41b

pre-exposure, 4-41a

reservoir, 4-38b

signs and symptoms, 4-42b

transmission, 4-38c

treatment, 4-44

triage, 4-44a

therapy, 1-13

toxins, 4-1

clostridium botulinum, 4-2

clostridium perfringens, 4-11

ricin, 4-20

saxitoxin, 4-29

staphylococcal enterotoxin B, 4-38

trichothecene mycotoxins, 4-47

trichothecene mycotoxins, 4-47

agent delivery, 4-48

clinical presentation, 4-51

control of patients, contacts, and treatment areas, 4-54

detection, 4-49

diagnosis, 4-52

endemic disease, 4-47d

etiologic agent, 4-47a

evacuation, 4-55

incubation period, 4-51a

medical management, 4-53b

prevention, 4-50

antivesicant cream or ointment, 4-50a

prognosis, 4-53c

prophylaxis, 4-50

post-exposure, 4-50b

pre-exposure, 4-50a

reservoir, 4-47b

signs and symptoms, 4-51b
Index-9

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

transmission, 4-47c

treatment, 4-53

triage, 4-53a

tularemia, 2-57

agent delivery, 2-58

clinical presentation, 2-61

control of patients, contacts, and treatment areas, 2-64

detection, 2-59

diagnosis, 2-62

endemic disease, 2-57d

etiologic agent, 2-57

evacuation, 2-65

incubation period, 2-61a

medical management, 2-63b

prevention, 2-60

miscellaneous, 2-60a

prognosis, 2-63c

prophylaxis, 2-60

post-exposure, 2-60c

pre-exposure, 2-60b

reservoir, 2-57b

signs and symptoms, 2-61b

transmission, 2-57c

treatment, 2-63

triage, 2-63a

Venezuelan equine encephalitis, 3-11

agent delivery, 3-12

clinical presentation, 3-15

control of patients, contacts, and treatment areas, 3-18

detection, 3-13

diagnosis, 3-16

endemic disease, 3-11d

etiologic agent, 3-11a

evacuation, 3-19

incubation period, 3-15a

medical management, 3-17b

prevention, 3-14

immunization, 3-14a

prognosis, 3-17c

prophylaxis, 3-14

post-exposure, 3-14b

pre-exposure, 3-14a

reservoir, 3-11b

signs and symptoms, 3-15b

transmission, 3-11c
Index-10

FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

treatment, 3-17

triage, 3-17a

viral

agents, 3-1

smallpox, 3-2

Venezuelan equine encephalitis, 3-11

viral hemorrhagic fevers, 3-20

hemorrhagic fevers, 3-20

agent delivery, 3-21

clinical presentation, 3-24

control of patients, contacts, and treatment areas, 3-27

detection, 3-22

diagnosis, 3-25

endemic disease, 3-20b

etiologic agent, 3-20a

evacuation, 3-28

incubation period, 3-24a

infectious material handling, 3-27d

isolation, 3-27b

medical management, 3-26b

prevention, 3-23

immunizations, 3-23a, b

prognosis, 3-26c

prophylaxis, 3-23

post-exposure, 3-23b

pre-exposure, 3-23a

reservoir, Table 3-1

signs and symptoms, 3-24b

transmission, 3-20a

treatment, 3-26

triage, 3-26a

World Health Organization, 1-21b(3)(c)
FM 8-284/NAVMED P-5042/AFMAN (I) 44-156/MCRP 4-11.1C

By Order of the Secretary of the Army:

ERIC K. SHINSEKI

Official: General, United States Army

Chief of Staff

JOEL B. HUDSON

Administrative Assistant to the

Secretary of the Army

By Order of the Secretary of the Navy:

R. A. NELSON

Vice Admiral, Medical Corps

United States Navy

Official: Chief, Bureau of Medicine and Surgery

By Order of the Secretary of the Air Force:

MICHAEL E. RYAN

General, USAF

Official: Chief of Staff

PAUL K. CARLTON, JR

Lieutenant General, USAF, MC, CFS

Surgeon General

By Direction of the Commandant of the Marine Corps:

J. E. RHODES

Lieutenant General, US Marine Corps

Commanding General

Marine Corps Combat Development Command

Official:

DISTRIBUTION:

US Army: Active Army, USAR, and ARNG: To be distributed in accordance with the initial

distribution number 115795, requirements for FM 8-284.

US Navy: All Ships and Stations having Medical Department Personnel.

US Air Force: F

US Marine Corps: PCN: 14400008000

*U.S. Government Printing Office: 2000  466-977
PCN: 14400008000