Federation of American Scientists :: Biological Threat Agents Information
Federation of American Scientists :: Biological Threat Agents Information
Brucellosis
Brucellosis is a systemic zoonotic disease that, in humans, is caused by one of four species of bacteria: Brucella melitensis, B. abortus, B. suis, and B. canis; virulence for humans decreases somewhat in the order given. These bacteria are small gram-negative, aerobic, non-motile coccobacilli that grow within monocytes and macrophages. They reside quiescently in tissue and bone-marrow, and are extremely difficult to eradicate even with antibiotic therapy. Their natural reservoir is domestic animals, such as goats, sheep, and camels (B. melitensis); cattle (B. abortus); and pigs (B. suis). Brucella canis is primarily a pathogen of dogs, and only occasionally causes disease in humans upon contact with an infected dog's blood, semen, or placenta. Humans are infected when they ingest raw (unpasteurized), infected milk or meat, inhale contaminated aerosols, or have abraded skin or conjunctival surfaces that come in contact with the bacteria. Laboratory infections are quite common, but human-to-human transmission is rare, occurring through breastfeeding. Therefore, isolation of infected patients is not required. Brucella species long have been considered potential candidates for use in biological warfare. The organisms are readily lyophilized, perhaps enhancing their infectivity. Under selected environmental conditions (for example, darkness, cool temperatures, high CO2), persistence for up to 2 years has been documented. When used as a biological warfare agent, Brucellae would most likely be delivered by the aerosol route; the resulting infection would be expected to mimic natural disease.
Brucellosis presents after an incubation period normally ranging from 3-4 weeks, but may be as short as 1 week or as long as several months. Clinical disease presents typically as an acute, non-specific febrile illness with chills, sweats, headache, fatigue, myalgias, arthralgias, and anorexia. Cough occurs in 15-25%, but the chest x-ray usually is normal. Complications include sacroiliitis, arthritis, vertebral osteomyelitis, epididymo-orchitis, and rarely endocarditis. Physical findings include lymphadenopathy in 10-20% and splenomegaly in 20-30% of cases. Untreated disease can persist for months to years, often with relapses and remissions. Disability may be pronounced. Lethality may approach 6% following infection with B. melitensis, but the disease is rarely fatal (0.5% or less) after infection with other serotypes (usually after endocarditis develops).
The initial symptoms of brucellosis are usually nonspecific, and the differential diagnosis is therefore very broad and includes bacterial, viral, and mycoplasmal infections. The systemic symptoms of viral and mycoplasmal illnesses, however, are usually present for only a few days, while they persist for prolonged periods in brucellosis. Brucellosis may be indistinguishable clinically from the typhoidal form of tularemia or from typhoid fever itself. The disease in humans is characterized by a multitude of somatic complaints, including fever, sweats, anorexia, fatigue, malaise, weight loss, and depression. Localized complications may involve the cardiovascular, gastrointestinal, genitourinary, hepatobiliary, osteoarticular, pulmonary and nervous systems. Without adequate and prompt antibiotic treatment, some patients develop a ‘chronic’ brucellosis syndrome with many features of the ‘chronic fatigue’ syndrome.
The recommended treatment is doxycycline (200 mg/day) plus rifampin (900 mg/day) for 6 weeks. Alternative effective treatment consists of doxycycline (200 mg/day) for 6 weeks plus streptomycin (1 gm/day) for 3 weeks. Trimethoprimsulfamethoxazole given for 4-6 weeks is less effective. In 5-10% of cases, there may be relapse or treatment failure. Laboratory infections with brucellosis are quite common, but there is no human-to-human transmission and isolation is not required.
Killed and live attenuated human vaccines of unproven efficacy have been available in many countries, but not in the U.S. and many parts of Europe. There is no information on the use of antibiotics for prophylaxis against human brucellosis.
Cholera
Cholera is a diarrheal disease caused by Vibrio cholera, a short, curved, gram-negative bacillus. Humans acquire the disease by consuming water or food contaminated with the organism. The organism multiplies in the small intestine and secretes an enterotoxin that causes a secretory diarrhea. When employed as a BW agent, cholera will most likely be used to contaminate water supplies. It is unlikely to be used in aerosol form. Without treatment, death may result from severe dehydration, hypovolemia and shock. Vomiting is often present early in the illness and may complicate oral replacement of fluid losses. There is little or no fever or abdominal pain.
Watery diarrhea can also be caused by enterotoxigenic E. coli, rotavirus or other viruses, noncholera Vibrios, or food poisoning due to ingestion of preformed toxins such as those of Clostridium perfringens, Bacillus cereus, or Staphylococcus aureus.
Treatment of cholera depends primarily on replacement of fluid and electrolyte losses. This is best accomplished using oral dehydration therapy with the World Health Organization solution (3.5 g NaCl, 2.5 g NaHC03, 1.5 g KC1 and 20 g glucose per liter). Intravenous fluid replacement is occasionally needed when vomiting is severe, when the volume of stool output exceeds 7 liters/day, or when severe dehydration with shock has developed. Antibiotics will shorten the duration of diarrhea and thereby reduce fluid losses.
Improved oral cholera vaccines are presently being tested. One vaccine, which has been discontinued in the U.S., is a killed suspension of V. cholera provided about 50% protection that lasts for no more than 6 months. The initial dose is two injections given at least 1 week apart with booster doses every 6 months.
Ebola Hemorrhagic Fever
Ebola hemorrhagic fever is one of the most virulent viral diseases known to humankind, causing death in 50-90% of all clinically-ill cases. Consequently, it has figured prominently in popular discussions of biological weapons, although its practical applications as a biological threat agent remain speculative. The disease has its origins in the jungles of Africa and Asia and several different forms of Ebola virus have been identified and may be associated with other clinical expressions, on which further research is required.
The Ebola virus is transmitted by direct contact with the blood, secretions, organs or semen of infected persons. Transmission through semen may occur up to 7 weeks after clinical recovery, as with Marburg hemorrhagic fever. Health care workers have frequently been infected while attending patients. In the 1976 epidemic in Zaire, every Ebola case caused by contaminated syringes and needles died.
After an incubation period of 2 to 21 days, Ebola is often characterized by the sudden onset of fever, weakness, muscle pain, headache and sore throat. This is followed by vomiting, diarrhea, rash, limited kidney and liver functions, and both internal and external bleeding. Specialized laboratory tests on blood specimens (which are not commercially available) detect specific antigens or antibodies and/or isolate the virus. These tests present an extreme biohazard and are only conducted under maximum containment conditions.
No specific treatment or vaccine exists for Ebola hemorrhagic fever. Severe cases require intensive supportive care, as patients are frequently dehydrated and in need of intravenous fluids. Experimental studies involving the use of hyperimmune sera on animals demonstrated no long-term protection against the disease after interruption of therapy.
Suspected cases should be isolated from other patients and strict barrier nursing techniques practiced. All hospital personnel should be briefed on the nature of the disease and its routes of transmission. Particular emphasis should be placed on ensuring that high-risk procedures such as the placing of intravenous lines and the handling of blood, secretions, catheters, and suction devices are done under barrier nursing conditions. Hospital staff should have individual gowns, gloves, and masks. Gloves and masks must not be reused unless disinfected. Patients who die from the disease should be promptly buried or cremated.
As the primary mode of person-to-person transmission is contact with contaminated blood, secretion, or body fluids, any person who has had close physical contact with patients should be kept under strict surveillance, i.e. body temperature checks twice a day, with immediate hospitalization and strict isolation recommended in case of temperatures above 38.3° C (101° F). Casual contacts should be placed on alert and asked to report any fever. Surveillance of suspected cases should continue for three weeks after the date of their last contact. Hospital personnel who come into close contact with patients or contaminated materials without barrier nursing attire must be considered exposed and put under close supervised surveillance.
The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby region of Zaire in 1976 after significant epidemics in Yamkubu, northern Zaire, and Nzara, southern Sudan. Between June and November 1976 the Ebola virus infected 284 people in Sudan, with 117 deaths. In Zaire there were 318 cases and 280 deaths in September and October. An isolated case occurred in Zaire in 1977 and a second outbreak in Sudan in 1979. In 1989 and 1990, a filovirus, named Ebola-Reston, was isolated in monkeys being held in quarantine in laboratories in Reston, VA, Alice, TX, and Pennsylvania. In the Philippines, Ebola-Reston infections occurred in a quarantine area near Manila for monkeys intended for exportation. A large epidemic occurred in Kikwit, Zaire in 1995 with 315 cases, 244 with fatal outcomes. One human case of Ebola hemorrhagic fever and several cases in chimpanzees were confirmed in Côte d'Ivoire in 1994-95. In Gabon, Ebola hemorrhagic fever was first documented in 1994 and recent outbreaks occurred in February 1996 and July 1996. In all, nearly 1,100 cases with 793 deaths have been documented since the virus was discovered. The natural reservoir of the Ebola virus seems to reside in the rain forests of Africa and Asia but has not yet been identified.
Different hypotheses have been developed to try to uncover the cycle of Ebola. Initially, rodents were suspected, as is the case with Lassa Fever whose reservoir is a wild rodent (Mastomys). Another hypothesis is that a plant virus may have caused the infection of vertebrates. Laboratory observation has shown that bats experimentally infected with Ebola do not die and this has raised speculation that these mammals may play a role in maintaining the virus in the tropical forest.
Tularemia
Tularemia is a zoonotic disease caused by Francisella tularensis, a gram-negative bacillus. Humans acquire the disease under natural conditions through inoculation of skin or mucous membranes with blood or tissue fluids of infected animals, or bites of infected deerflies, mosquitoes, or ticks. A BW attack with F. tularensis delivered by aerosol would primarily cause typhoidal tularemia, a syndrome expected to have a case fatality rate which may be higher than the 5-10% seen when disease is acquired naturally.
A variety of clinical forms of tularemia are seen, depending upon the route of inoculation and virulence of the strain. In humans, as few as 10-50 organisms will cause disease if inhaled or injected intradermally, whereas 108 organisms are required with oral challenge. Under natural conditions, ulceroglandular tularemia generally occurs about 3 days after intradermal inoculation (range 2-10 days), and manifests as regional lymphadenopathy, fever, chills, headache, and malaise, with or without a cutaneous ulcer. Gastrointestinal tularemia occurs after drinking contaminated ground water, and is characterized by abdominal pain, nausea, vomiting, and diarrhea. Bacteremia may be common after primary intradermal, respiratory, or gastrointestinal infection with F. tularensis and could result in septicemia or "typhoidal" tularemia. The typhoidal form also may occur as a primary condition in 5-15% of naturally-occurring cases; clinical features include fever, prostration, and weight loss, but without adenopathy. Diagnosis of primary typhoidal tularemia is difficult, as signs and symptoms are nonspecific and there frequently is no suggestive exposure history. Pneumonic tularemia is a severe atypical pneumonia that may be fulminant, and can be primary or secondary. Primary pneumonia may follow direct inhalation of infectious aerosols, or may result from aspiration of organisms in cases of pharyngeal tularemia. Pneumonic tularemia causes fever, headache, malaise, substernal discomfort, and a non-productive cough; radiologic evidence of pneumonia or mediastinal lymphadenopathy may or may not be present. A biological warfare attack with F. tularensis would most likely be delivered by aerosol, causing primarily typhoidal tularemia. Many exposed individuals would develop pneumonic tularemia (primary or secondary), but clinical pneumonia may be absent or non-evident. Case fatality rates may be higher than the 5-10% seen when the disease is acquired naturally.
The clinical presentation of tularemia may be severe, yet nonspecific. Differential diagnoses include typhoidal syndromes (e.g., salmonella, rickettsia, malaria) or pneumonic processes (e.g., plague, mycoplasma, SEB). A clue to the diagnosis of tularemia delivered as a BW agent might be a large number of temporally clustered patients presenting with similar systemic illnesses, a proportion of whom will have a nonproductive pneumonia. Identification of organisms by staining ulcer fluids or sputum is generally not helpful. Routine culture is difficult, due to unusual growth requirements and/or overgrowth of commensal bacteria.
Streptomycin (1 gm every 12 hours intramuscularly (IM) for 10-14 days) is the treatment of choice. Gentamicin also is effective (3-5 mg/kg/day parenterally for 10-14 days). Tetracycline and chloramphenicol treatment are effective as well, but are associated with a significant relapse rate. Although laboratory-related infections with this organism are very common, human-to-human spread is unusual and isolation is not required.
A live, attenuated tularemia vaccine is available as an investigational new drug (IND). This vaccine has been administered to more than 5,000 persons without significant adverse reactions and is of proven effectiveness in preventing laboratory-acquired typhoidal tularemia. Its effectiveness against the concentrated bacterial challenge expected in a BW attack is unproven. The use of antibiotics for prophylaxis against tularemia is controversial.
Biological and Chemical Agents Factsheets
1918 Influenza A (H1N1)
Avian Influenza A (H5N1)
Anthrax
Botulinum Toxin
Cyanide
Ebola
Ricin
Salmonella
Sarin
Smallpox
Tularemia
White Phosphorus
Federation of American Scientists :: Biological Threat Agents Information
Brucellosis
Brucellosis is a systemic zoonotic disease that, in humans, is caused by one of four species of bacteria: Brucella melitensis, B. abortus, B. suis, and B. canis; virulence for humans decreases somewhat in the order given. These bacteria are small gram-negative, aerobic, non-motile coccobacilli that grow within monocytes and macrophages. They reside quiescently in tissue and bone-marrow, and are extremely difficult to eradicate even with antibiotic therapy. Their natural reservoir is domestic animals, such as goats, sheep, and camels (B. melitensis); cattle (B. abortus); and pigs (B. suis). Brucella canis is primarily a pathogen of dogs, and only occasionally causes disease in humans upon contact with an infected dog's blood, semen, or placenta. Humans are infected when they ingest raw (unpasteurized), infected milk or meat, inhale contaminated aerosols, or have abraded skin or conjunctival surfaces that come in contact with the bacteria. Laboratory infections are quite common, but human-to-human transmission is rare, occurring through breastfeeding. Therefore, isolation of infected patients is not required. Brucella species long have been considered potential candidates for use in biological warfare. The organisms are readily lyophilized, perhaps enhancing their infectivity. Under selected environmental conditions (for example, darkness, cool temperatures, high CO2), persistence for up to 2 years has been documented. When used as a biological warfare agent, Brucellae would most likely be delivered by the aerosol route; the resulting infection would be expected to mimic natural disease.
Brucellosis presents after an incubation period normally ranging from 3-4 weeks, but may be as short as 1 week or as long as several months. Clinical disease presents typically as an acute, non-specific febrile illness with chills, sweats, headache, fatigue, myalgias, arthralgias, and anorexia. Cough occurs in 15-25%, but the chest x-ray usually is normal. Complications include sacroiliitis, arthritis, vertebral osteomyelitis, epididymo-orchitis, and rarely endocarditis. Physical findings include lymphadenopathy in 10-20% and splenomegaly in 20-30% of cases. Untreated disease can persist for months to years, often with relapses and remissions. Disability may be pronounced. Lethality may approach 6% following infection with B. melitensis, but the disease is rarely fatal (0.5% or less) after infection with other serotypes (usually after endocarditis develops).
The initial symptoms of brucellosis are usually nonspecific, and the differential diagnosis is therefore very broad and includes bacterial, viral, and mycoplasmal infections. The systemic symptoms of viral and mycoplasmal illnesses, however, are usually present for only a few days, while they persist for prolonged periods in brucellosis. Brucellosis may be indistinguishable clinically from the typhoidal form of tularemia or from typhoid fever itself. The disease in humans is characterized by a multitude of somatic complaints, including fever, sweats, anorexia, fatigue, malaise, weight loss, and depression. Localized complications may involve the cardiovascular, gastrointestinal, genitourinary, hepatobiliary, osteoarticular, pulmonary and nervous systems. Without adequate and prompt antibiotic treatment, some patients develop a ‘chronic’ brucellosis syndrome with many features of the ‘chronic fatigue’ syndrome.
The recommended treatment is doxycycline (200 mg/day) plus rifampin (900 mg/day) for 6 weeks. Alternative effective treatment consists of doxycycline (200 mg/day) for 6 weeks plus streptomycin (1 gm/day) for 3 weeks. Trimethoprimsulfamethoxazole given for 4-6 weeks is less effective. In 5-10% of cases, there may be relapse or treatment failure. Laboratory infections with brucellosis are quite common, but there is no human-to-human transmission and isolation is not required.
Killed and live attenuated human vaccines of unproven efficacy have been available in many countries, but not in the U.S. and many parts of Europe. There is no information on the use of antibiotics for prophylaxis against human brucellosis.
Cholera
Cholera is a diarrheal disease caused by Vibrio cholera, a short, curved, gram-negative bacillus. Humans acquire the disease by consuming water or food contaminated with the organism. The organism multiplies in the small intestine and secretes an enterotoxin that causes a secretory diarrhea. When employed as a BW agent, cholera will most likely be used to contaminate water supplies. It is unlikely to be used in aerosol form. Without treatment, death may result from severe dehydration, hypovolemia and shock. Vomiting is often present early in the illness and may complicate oral replacement of fluid losses. There is little or no fever or abdominal pain.
Watery diarrhea can also be caused by enterotoxigenic E. coli, rotavirus or other viruses, noncholera Vibrios, or food poisoning due to ingestion of preformed toxins such as those of Clostridium perfringens, Bacillus cereus, or Staphylococcus aureus.
Treatment of cholera depends primarily on replacement of fluid and electrolyte losses. This is best accomplished using oral dehydration therapy with the World Health Organization solution (3.5 g NaCl, 2.5 g NaHC03, 1.5 g KC1 and 20 g glucose per liter). Intravenous fluid replacement is occasionally needed when vomiting is severe, when the volume of stool output exceeds 7 liters/day, or when severe dehydration with shock has developed. Antibiotics will shorten the duration of diarrhea and thereby reduce fluid losses.
Improved oral cholera vaccines are presently being tested. One vaccine, which has been discontinued in the U.S., is a killed suspension of V. cholera provided about 50% protection that lasts for no more than 6 months. The initial dose is two injections given at least 1 week apart with booster doses every 6 months.
Ebola Hemorrhagic Fever
Ebola hemorrhagic fever is one of the most virulent viral diseases known to humankind, causing death in 50-90% of all clinically-ill cases. Consequently, it has figured prominently in popular discussions of biological weapons, although its practical applications as a biological threat agent remain speculative. The disease has its origins in the jungles of Africa and Asia and several different forms of Ebola virus have been identified and may be associated with other clinical expressions, on which further research is required.
The Ebola virus is transmitted by direct contact with the blood, secretions, organs or semen of infected persons. Transmission through semen may occur up to 7 weeks after clinical recovery, as with Marburg hemorrhagic fever. Health care workers have frequently been infected while attending patients. In the 1976 epidemic in Zaire, every Ebola case caused by contaminated syringes and needles died.
After an incubation period of 2 to 21 days, Ebola is often characterized by the sudden onset of fever, weakness, muscle pain, headache and sore throat. This is followed by vomiting, diarrhea, rash, limited kidney and liver functions, and both internal and external bleeding. Specialized laboratory tests on blood specimens (which are not commercially available) detect specific antigens or antibodies and/or isolate the virus. These tests present an extreme biohazard and are only conducted under maximum containment conditions.
No specific treatment or vaccine exists for Ebola hemorrhagic fever. Severe cases require intensive supportive care, as patients are frequently dehydrated and in need of intravenous fluids. Experimental studies involving the use of hyperimmune sera on animals demonstrated no long-term protection against the disease after interruption of therapy.
Suspected cases should be isolated from other patients and strict barrier nursing techniques practiced. All hospital personnel should be briefed on the nature of the disease and its routes of transmission. Particular emphasis should be placed on ensuring that high-risk procedures such as the placing of intravenous lines and the handling of blood, secretions, catheters, and suction devices are done under barrier nursing conditions. Hospital staff should have individual gowns, gloves, and masks. Gloves and masks must not be reused unless disinfected. Patients who die from the disease should be promptly buried or cremated.
As the primary mode of person-to-person transmission is contact with contaminated blood, secretion, or body fluids, any person who has had close physical contact with patients should be kept under strict surveillance, i.e. body temperature checks twice a day, with immediate hospitalization and strict isolation recommended in case of temperatures above 38.3° C (101° F). Casual contacts should be placed on alert and asked to report any fever. Surveillance of suspected cases should continue for three weeks after the date of their last contact. Hospital personnel who come into close contact with patients or contaminated materials without barrier nursing attire must be considered exposed and put under close supervised surveillance.
The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby region of Zaire in 1976 after significant epidemics in Yamkubu, northern Zaire, and Nzara, southern Sudan. Between June and November 1976 the Ebola virus infected 284 people in Sudan, with 117 deaths. In Zaire there were 318 cases and 280 deaths in September and October. An isolated case occurred in Zaire in 1977 and a second outbreak in Sudan in 1979. In 1989 and 1990, a filovirus, named Ebola-Reston, was isolated in monkeys being held in quarantine in laboratories in Reston, VA, Alice, TX, and Pennsylvania. In the Philippines, Ebola-Reston infections occurred in a quarantine area near Manila for monkeys intended for exportation. A large epidemic occurred in Kikwit, Zaire in 1995 with 315 cases, 244 with fatal outcomes. One human case of Ebola hemorrhagic fever and several cases in chimpanzees were confirmed in Côte d'Ivoire in 1994-95. In Gabon, Ebola hemorrhagic fever was first documented in 1994 and recent outbreaks occurred in February 1996 and July 1996. In all, nearly 1,100 cases with 793 deaths have been documented since the virus was discovered. The natural reservoir of the Ebola virus seems to reside in the rain forests of Africa and Asia but has not yet been identified.
Different hypotheses have been developed to try to uncover the cycle of Ebola. Initially, rodents were suspected, as is the case with Lassa Fever whose reservoir is a wild rodent (Mastomys). Another hypothesis is that a plant virus may have caused the infection of vertebrates. Laboratory observation has shown that bats experimentally infected with Ebola do not die and this has raised speculation that these mammals may play a role in maintaining the virus in the tropical forest.
Tularemia
Tularemia is a zoonotic disease caused by Francisella tularensis, a gram-negative bacillus. Humans acquire the disease under natural conditions through inoculation of skin or mucous membranes with blood or tissue fluids of infected animals, or bites of infected deerflies, mosquitoes, or ticks. A BW attack with F. tularensis delivered by aerosol would primarily cause typhoidal tularemia, a syndrome expected to have a case fatality rate which may be higher than the 5-10% seen when disease is acquired naturally.
A variety of clinical forms of tularemia are seen, depending upon the route of inoculation and virulence of the strain. In humans, as few as 10-50 organisms will cause disease if inhaled or injected intradermally, whereas 108 organisms are required with oral challenge. Under natural conditions, ulceroglandular tularemia generally occurs about 3 days after intradermal inoculation (range 2-10 days), and manifests as regional lymphadenopathy, fever, chills, headache, and malaise, with or without a cutaneous ulcer. Gastrointestinal tularemia occurs after drinking contaminated ground water, and is characterized by abdominal pain, nausea, vomiting, and diarrhea. Bacteremia may be common after primary intradermal, respiratory, or gastrointestinal infection with F. tularensis and could result in septicemia or "typhoidal" tularemia. The typhoidal form also may occur as a primary condition in 5-15% of naturally-occurring cases; clinical features include fever, prostration, and weight loss, but without adenopathy. Diagnosis of primary typhoidal tularemia is difficult, as signs and symptoms are nonspecific and there frequently is no suggestive exposure history. Pneumonic tularemia is a severe atypical pneumonia that may be fulminant, and can be primary or secondary. Primary pneumonia may follow direct inhalation of infectious aerosols, or may result from aspiration of organisms in cases of pharyngeal tularemia. Pneumonic tularemia causes fever, headache, malaise, substernal discomfort, and a non-productive cough; radiologic evidence of pneumonia or mediastinal lymphadenopathy may or may not be present. A biological warfare attack with F. tularensis would most likely be delivered by aerosol, causing primarily typhoidal tularemia. Many exposed individuals would develop pneumonic tularemia (primary or secondary), but clinical pneumonia may be absent or non-evident. Case fatality rates may be higher than the 5-10% seen when the disease is acquired naturally.
The clinical presentation of tularemia may be severe, yet nonspecific. Differential diagnoses include typhoidal syndromes (e.g., salmonella, rickettsia, malaria) or pneumonic processes (e.g., plague, mycoplasma, SEB). A clue to the diagnosis of tularemia delivered as a BW agent might be a large number of temporally clustered patients presenting with similar systemic illnesses, a proportion of whom will have a nonproductive pneumonia. Identification of organisms by staining ulcer fluids or sputum is generally not helpful. Routine culture is difficult, due to unusual growth requirements and/or overgrowth of commensal bacteria.
Streptomycin (1 gm every 12 hours intramuscularly (IM) for 10-14 days) is the treatment of choice. Gentamicin also is effective (3-5 mg/kg/day parenterally for 10-14 days). Tetracycline and chloramphenicol treatment are effective as well, but are associated with a significant relapse rate. Although laboratory-related infections with this organism are very common, human-to-human spread is unusual and isolation is not required.
A live, attenuated tularemia vaccine is available as an investigational new drug (IND). This vaccine has been administered to more than 5,000 persons without significant adverse reactions and is of proven effectiveness in preventing laboratory-acquired typhoidal tularemia. Its effectiveness against the concentrated bacterial challenge expected in a BW attack is unproven. The use of antibiotics for prophylaxis against tularemia is controversial.
Biological and Chemical Agents Factsheets
1918 Influenza A (H1N1)
Avian Influenza A (H5N1)
Anthrax
Botulinum Toxin
Cyanide
Ebola
Ricin
Salmonella
Sarin
Smallpox
Tularemia
White Phosphorus
Federation of American Scientists :: Biological Threat Agents Information
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