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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, 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.
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 Wrights 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. Administer ciprofloxacin 500 mg orally every 12 hours or
doxycycline 100 mg orally every 12 hours beginning when a BW attack is imminent or suspected; discontinue
if the employment of plague BW can be excluded.
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, gram-
negative 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 hosts
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.
Chemoprophylaxis given for anthrax or plague (ciprofloxacin, doxycycline) may confer
protection against tularemia, based on in vitro susceptibilities.
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-to-
face 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 flat-
type 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.
4-5
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