• Gram positive sporulating bacillus
• Reservoir is the soil; distribution is worldwide
• Exists in host as vegetative bacillus and in environment as a spore
• Spores can survive adverse environmental conditions and remain viable for decades
• 3 clinical presentations in humans: cutaneous, GI, and inhalational
• Cutaneous Disease
• Develops 2-5 days after exposure
• Begins as a papule which becomes vesicular in 24-48 hours
• Lesions sometimes pruritic but never painful
• Lesion ruptures in 1 week, leaving an ulcer that becomes a black eschar
• Fever, HA, malaise, regional lymphadenopathy may be present
• 5-20% fatality if untreated; < 1% if treated
• GI Disease
• Develops 2-5 days after exposure
• Symptoms include abdominal pain, hematemesis, melena and/or hematochezia, ascites, profuse diarrhea
• Mortality high
• Inhalation Disease
• Develops 1-6 days after exposure
• Symptoms include fever, nonproductive cough, myalgias
• Abrupt onset of respiratory distress characterized by dyspnea, stridor, diaphoresis, and cyanosis
• Bacteremia and septic shock can result in death in less than 24 hours
• Almost uniformally fatal since treatment not effective after symptoms present
• Complicated by meningitis in up to 50% of cases
• Differential includes tularemia, plague, cutaneous diphtheria, staphylococcal disease, and rickettsial infection
• Diagnosis : Wright or Gram stain of blood or by blood culture
• Treatment : Cipro, doxycycline, or penicillin
• Chemoprophylactic and vaccination regimens exist

1. Smallpox (Variola)

• Last natural case in Somalia 1977; declared eradicated in 1980
• Easily produced in large quantities and can be freeze-dried, preserving virulence for months to years
• No mild or subclinical infection in unimmunized person
• Mortality 25-30%
• Most likely only 10-15% population has residual smallpox immunity
• Only 5-10 million doses of smallpox vaccine in U.S. and no production facilities exist
• After aerosol exposure, travels from respiratory tract to regional lymph nodes and replicates producing viremia
• Rash develops as well as malaise, fever, rigors, emesis, HA, backache
• 2-3 days later enanthem appears with rash on face, hands and forearms
• Mucous membrane lesions occur leading to transmission
• Rash then spreads centrally
• Differential includes vesicular exanthems such as chickenpox, erythema multiforme with bullae, or allergic contact dermatitis
• Treatment : none proven, possibly cidofovir

1. Plague

• Y. pestis , a gram negative bacillus maintained in rodent reservoirs
• Transmitted from rodent to humans via fleas and animal to human and human to human via respiratory droplets
• Clinical presentations are bubonic, primary septicemic, and pneumonic
• Incubation 2-3 days, followed by pneumonia, malaise, high fever, chills, HA, myalgias, hemoptysis, and sepsis
• CXR reveals patchy or consolidated brochopneumonia
• Pneumonic plague progresses rapidly resulting in dsypnea, stridor, cyanosis, respiratory failure, shock and death
• Diagnosis: Wright-Geimsa stain, immunofluorescent stain or culture
• Treatment: Streptomycin, tetracycline, chloramphenicol, gentamicin, doxycycline (pneumonic plague almost always fatal if treatment not given within 24 hours of symptom onset)
• Vaccine available against bubonic plague, most likely poor efficacy against pneumonic plague

1. Q Fever

• Febrile, zoonotic disease caused by Coxiella burnetti, an obligate intracellular rickettsialike organism
• Produces a sporelike form that can withstand heat and drying
• Infectivity and morbidity similar to anthrax, though rarely lethal
• Clinically presents as fever, chills, HA, diaphoresis, malaise, fatigue, anorexia
• Rales often noted, and rarely hepatomegaly, splenomegaly and jaundice
• Lab findings include increased LFTs, normal WBC count, mild anemia, and occasional thrombocytopenia
• Serologic testing used for diagnosis
• Treatment: tetracyclines and macrolides
• Vaccine investigational in US

1. Tularemia

• Aerobic, gram negative coccobacillus, Francisella tularensis
• Zoonotic disease
• Also called rabbit fever and deer fly fever
• Respiratory exposure would cause typhoidal tularemia
• Organism can remain viable in environment for weeks and in frozen meet for years
• Can occur in humans in 2 forms: ulceroglandular and typhoidal
• Typhoidal tularemia manifests as fever, prostration, and weight lost without adenopathy
• CXR shows pneumonia and possibly pleural effusions
• Untreated typhoidal tularemia has a fatality rate of 35%
• Diagnosis: difficult since symptoms non-specific but culturing or serologic testing can be done
• Treatment: Streptomycin, getamicin (tetracycline and chloramphenicol can be used but reactivation higher)
• Human to human transmission unusual
• Vaccine available as investigational drug

1. Viral Encephalitides

• Alphavirus genus of Togaviridae including Venezuelan, Eastern, and Western equine encephalitis viruses (VEE, EEE, WEE)
• Highly infectious by aerosol
• Can be produced in large amounts, are inexpensive, and very stable during storage
• Can readily produce incapacitating or lethal infection and can be easily genetically manipulated
• Majority of infections manifested as systemic, viral febrile syndromes consisting of HA, fever and myalgias
• Progress to confusion, obtundation, dysphasia, seizures, paresis, ataxia, myoclonus, and/or cranial nerve palsies
• EEE most severe with fatality rates of 50 -75% (30% of survivors have neurological sequelae)
• Diagnosis: virus isolation or serologic testing
• Treatment: none
• Vaccines do exist

1. Viral Hemorrhagic Fevers (VHF)

• Caused by a variety of RNA viruses
• VHF is an acute febrile illness characterized by malaise, prostration and generalized signs of vascular permeability
• Viruses highly infectious by aerosol with high morbidity and mortality
• Include Lassa fever, AHF, BHF, VHF, RVF, CCHF, yellow fever, Hantavirus, Marburg disease and Ebola
• Mortality rates for Ebola 53-92%
• Common presentations include conjunctival injection, hypotension, flushing and petechial hemorrhage
• Full-blown VHF evolves to shock, mucus membrane hemorrhage and neurologic, hematopoietic, or pulmonary involvement
• DIC present with CCHF, Marburg and Ebola
• Diagnosis: ELISA or PCR, followed by cell culture and immunological identification
• Treatment: Ribavirin, antibody therapy
• Some vaccines exist

1. Botulinum Toxin

• Produced by Clostridium botulinum
• 7 distinct neurotoxins, A-G
• Can be inhaled or ingested
• Most toxic compound known; estimated toxic dose of 0.001 µg/kg body weight
• 15,000x more toxic than VX nerve gas and 100,000x more toxic than sarin gas
• Acts by binding to presynaptic nerve terminal at the neuromuscular junction (blocks neurotrasmission)
• Causes bulbar nerve palsies and skeletal muscle weakness
• Onset of symptoms from 24-36 hours up to several days
• Bulbar palsies result in blurred vision, mydriasis, diplopia, ptosis, photophobia, dysarthria, dysphonia, and dysphagia
• Skeletal muscle paralysis follows and may culminate in respiratory failure
• Can be confused with Guillian-Barré, myasthenia gravis, or tick paralysis
• Fatalities could be less than 5% with tracheostomy or endotrachael intubation
• Antitoxin effective if given before clinical signs develop
• Toxoid available

Breman JG and Henderson DA. Poxvirus dilemmas-monkeypox, smallpox and biological terrorism. NEJM. 1998; 339:556-559.

Christopher GW, et al. Biological warfare: a historical perspective. JAMA. 1997; 278:412-417.

Cole LA. The specter of biological weapons. Scientific American. 1996; Dec:60-65.

Franz DR, et al. clinical recognition and management of patients exposed to biological warfare agents. JAMA. 1997; 278:399-409.

Henderson DA. Bioterrorism as a public health threat. Emerging Infectious Diseases. 1998; 4:488-492.

Lesho E, et al. Feces, dead horses and fleas: evolution of the hostile use of biological agents. WJM. 1998; 168:512-516.

Pile JC, et al. Anthrax as a potential biological warfare agent. Arch Intern Med. 1998; 158:429-434.

Simon JD. Biological terrorism: preparing to meet the threat. JAMA. 1997; 278:428-430.

Zilinakas RA. Iraq’s biological weapons: the past as future? JAMA. 1997; 278:418-423.