Time: Thu Jul 17 07:19:14 1997
	by primenet.com (8.8.5/8.8.5) with ESMTP id HAA24442
	for [address in tool bar]; Thu, 17 Jul 1997 07:12:42 -0700 (MST)
	by usr04.primenet.com (8.8.5/8.8.5) with SMTP id HAA17253;
	Thu, 17 Jul 1997 07:11:58 -0700 (MST)
Date: Thu, 17 Jul 1997 07:11:32 -0700
To: (Recipient list suppressed)
From: Paul Andrew Mitchell [address in tool bar]
Subject: SLS: US Army clinical data on anthrax and plague (fwd)

>1 FEBRUARY 1996 
>B.02.   Anthrax. 
>    a.  Clinical Syndrome. 
>    (1)  Characteristics. Anthrax is a zoonotic disease caused by Bacillus
>anthracis. Under natural conditions,
>    humans become infected by contact with infected animals or contaminated
>animal products. Human anthrax is
>    usually manifested by cutaneous lesions. A biological warfare attack
>with anthrax spores delivered by aerosol
>    would cause inhalation anthrax, an extraordinarily rare form of the
>naturally occurring disease. 
>    (2)  Clinical Features. The disease begins after an incubation period
>varying from 1-6 days, presumably
>    dependent upon the dose of inhaled organisms. Onset is gradual and
>nonspecific, with fever, malaise, and fatigue,
>    sometimes in association with a nonproductive cough and mild chest
>discomfort. In some cases, there may be a
>    short period of improvement. The initial symptoms are followed in 2-3
>days by the abrupt development of severe
>    respiratory distress with dyspnea, diaphoresis, stridor, and cyanosis.
>Physical findings may include evidence of
>    pleural effusions, edema of the chest wall, and meningitis. Chest x-ray
>reveals a dramatically widened
>    mediastinum, often with pleural effusions, but typically without
>infiltrates. Shock and death usually follow within
>    24-36 hours of respiratory distress onset. 
>    b.  Diagnosis. 
>    (1)  Routine Laboratory Findings. Laboratory evaluation will reveal a
>neutrophilic leucocytosis. Pleural and
>    cerebrospinal fluids may be hemorrhagic. 
>    (2)  Differential Diagnosis. An epidemic of inhalation anthrax in its
>early stage with nonspecific symptoms could
>    be confused with a wide variety of viral, bacterial, and fungal
>infections. Progression over 2-3 days with the
>    sudden development of severe respiratory distress followed by shock and
>death in 24-36 hours in essentially all
>    untreated cases eliminates diagnoses other than inhalation anthrax. The
>presence of a widened mediastinum on
>    chest x-ray, in particular, should alert one to the diagnosis. Other
>suggestive findings include chest-wall edema,
>    hemorrhagic pleural effusions, and hemorrhagic meningitis. Other
>diagnoses to consider include aerosol exposure
>    to SEB; but in this case onset would be more rapid after exposure (if
>known), and no prodrome would be evident
>    prior to onset of severe respiratory symptoms. Mediastinal widening on
>chest x-ray will also be absent. Patients
>    with plague or tularemia pneumonia will have pulmonary infiltrates and
>clinical signs of pneumonia (usually absent
>    in anthrax). 
>    (3)  Specific Laboratory Diagnosis. Bacillus anthracis will be readily
>detectable by blood culture with routine
>    media. Smears and cultures of pleural fluid and abnormal cerebrospinal
>fluid may also be positive. Impression
>    smears of mediastinal lymph nodes and spleen from fatal cases should be
>positive. Toxemia is sufficient to permit
>    anthrax toxin detection in blood by immunoassays. 
>    c.  Therapy. Almost all cases of inhalation anthrax in which treatment
>was begun after patients were symptomatic
>    have been fatal, regardless of treatment. Historically, penicillin has
>been regarded as the treatment of choice, with
>    2 million units given intravenously every 2 hours. Tetracyclines and
>erythromycin have been recommended in
>    penicillin-sensitive patients. The vast majority of anthrax strains are
>sensitive in vitro to penicillin. However,
>    penicillin-resistant strains exist naturally, and one has been
>recovered from a fatal human case. Moreover, it is not
>    difficult to induce resistance to penicillin, tetracyclines,
>erythromycin, and many other antibiotics through
>    laboratory manipulation of organisms. All naturally occurring strains
>tested to date have been sensitive to
>    erythromycin, chloramphenicol, gentamicin, and ciprofloxacin. In the
>absence of information concerning antibiotic
>    sensitivity, treatment should be instituted at the earliest signs of
>disease with oral ciprofloxacin (1000 mg initially,
>    followed by 750 mg po (orally) bid (twice daily)) or intravenous
>doxycycline (200 mg initially, followed by 100
>    mg q (every) 12 hrs). Supportive therapy for shock, fluid volume
>deficit, and adequacy of airway may all be
>    needed. 
>    d.  Prophylaxis. 
>    (1)  Vaccine. A licensed, alum-precipitated preparation of purified B.
>anthracis protective antigen (PA) has been
>    shown to be effective in preventing or significantly reducing the
>incidence of inhalation anthrax. Limited human
>    data suggest that after completion of the first three doses of the
>recommended six-dose primary series (0, 2, 4
>    weeks, then 6, 12, 18 months), protection against both cutaneous and
>inhalation anthrax is afforded. Studies in
>    rhesus monkeys indicate that good protection is afforded after two
>doses (10-16 days apart) for up to 2 years. It
>    is likely that two doses in humans is protective as well, but there is
>too little information to draw firm conclusions.
>    As with all vaccines, the degree of protection depends upon the
>magnitude of the challenge dose; vaccine-induced
>    protection is undoubtedly overwhelmed by extremely high spore
>challenge. At least three doses of the vaccine (at
>    0, 2, and 4 weeks) are recommended for prophylaxis against inhalation
>anthrax. Contraindications for use are
>    sensitivity to vaccine components (formalin, alum, benzethonium
>chloride) and/or history of clinical anthrax.
>    Reactogenicity is mild to moderate: up to 6% of recipients will
>experience mild discomfort at the inoculation site
>    for up to 72 hours (tenderness, erythema, edema, pruritus), while a
>smaller proportion (<1%) will experience
>    more severe local reactions (potentially limiting use of the extremity
>for 1-2 days); modest systemic reactions
>    (myalgia, malaise, low-grade fever) are uncommon, and severe systemic
>reactions (anaphylaxis, which precludes
>    additional vaccination) are rare. The vaccine should be stored at
>refrigerator temperature (not frozen). 
>    (2)  Antibiotics. Choice of antibiotics for prophylaxis is guided by
>the same principles as that for treatment; i.e., it
>    is relatively easy to produce a penicillin-resistant organism in the
>laboratory, and possible, albeit somewhat more
>    difficult, to induce tetracycline resistance. Therefore, if there is
>information indicating that a biological weapon
>    attack is imminent, prophylaxis with ciprofloxacin (500 mg po bid), or
>doxycycline (100 mg po bid) is
>    recommended. If unvaccinated, a single 0.5 ml dose of vaccine should
>also be given subcutaneously. Should the
>    attack be confirmed as anthrax, antibiotics should be continued for at
>least 4 weeks in all exposed. In addition,
>    two 0.5 ml doses of vaccine should be given 2 weeks apart in the
>unvaccinated; those previously vaccinated with
>    fewer than three doses should receive a single 0.5 ml booster, while
>vaccination probably is not necessary for
>    those who have received the initial three doses within the previous 6
>months (primary series). Upon
>    discontinuation of antibiotics, patients should be closely observed; if
>clinical signs of anthrax occur, patients
>    should be treated as indicated above. If vaccine is not available,
>antibiotics should be continued beyond 4 weeks
>    until the patient can be closely observed upon discontinuation of
>B.09.  Plague. 
>    a.  Clinical Syndrome. 
>    (1)  Characteristics. Plague is a zoonotic disease caused by Yersinia
>pestis. Under natural conditions, humans
>    become infected as a result of contact with rodents, and their fleas.
>The transmission of the gram-negative
>    coccobacillus is by the bite of the infected flea, Xenopsylla cheopis,
>the oriental rat flea, or Pulex irritans, the
>    human flea. Under natural conditions, three syndromes are recognized:
>bubonic, primary septicemic, or
>    pneumonic. In a biological warfare scenario, the plague bacillus could
>be delivered via contaminated vectors
>    (fleas) causing the bubonic type or, more likely, via aerosol causing
>the pneumonic type. 
>    (2)  Clinical Features. In bubonic plague, the incubation period ranges
>from 2 to 10 days. The onset is acute and
>    often fulminant with malaise, high fever, and one or more tender lymph
>nodes. Inguinal lymphadenitis (bubo)
>    predominates, but cervical and axillary lymph nodes can also be
>involved. The involved nodes are tender,
>    fluctuant, and necrotic. Bubonic plague may progress spontaneously to
>the septicemic form with organisms spread
>    to the central nervous system, lungs (producing pneumonic disease), and
>elsewhere. The mortality is 50 percent in
>    untreated patients with the terminal event being circulatory collapse,
>hemorrhage, and peripheral thrombosis. In
>    primary pneumonic plague, the incubation period is 2 to 3 days. The
>onset is acute and fulminant with malaise,
>    high fever, chills, headache, myalgia, cough with production of a
>bloody sputum, and toxemia. The pneumonia
>    progresses rapidly, resulting in dyspnea, stridor, and cyanosis. In
>untreated patients, the mortality is 100 percent
>    with the terminal event being respiratory failure, circulatory
>collapse, and a bleeding diathesis. 
>    b.  Diagnosis. 
>    (1)  Presumptive. Presumptive diagnosis can be made by identification
>of the gram-negative coccobacillus with
>    safety-pin bipolar staining organisms in Giemsa or Wayson's stained
>slides from a lymph node needle aspirate,
>    sputum, or cerebrospinal fluid (CSF) samples. When available,
>immunofluorescent staining is very useful.
>    Elevated levels of antibody to Y. pestis in a nonvaccinated patient may
>also be useful. 
>    (2)  Definitive. Yersinia pestis can be readily cultured from blood,
>sputum, and bubo aspirates. Most naturally
>    occurring strains of Y. pestis produce an "Fl" antigen in vivo which
>can be detected in serum samples by
>    immunoassay. A fourfold rise of Y. pestis antibody levels in patient
>serum is also diagnostic. 
>    (3)  Differential. In cases where bubonic type is suspected, tularemia
>adenitis, staphylococcal or streptococcal
>    adenitis, meningococcemia, enteric gram-negative sepsis, and
>rickettsiosis need to be ruled out. In pneumonic
>    plague, tularemia, anthrax, and staphylococcal enterotoxin B (SEB)
>agents need to be considered. Continued
>    deterioration without stabilization effectively rules out SEB. The
>presence of a widened mediastinum on chest
>    x-ray should alert one to the diagnosis of anthrax. 
>    c.  Therapy. Plague may be spread from person to person by droplets.
>Strict isolation procedures for all cases are
>    indicated. Streptomycin, tetracycline, and chloramphenicol are highly
>effective if begun early. Significant
>    reduction in morbidity and mortality is possible if antibiotics are
>given within the first 24 hours after symptoms of
>    pneumonic plague develop. Intravenous doxycycline (200 mg initially,
>followed by 100 mg every 12 hours),
>    intramuscular streptomycin (1 g every 12 hours), or intravenous
>chloramphenicol (l g every 6 hours) for 10-14
>    days are effective against naturally occurring strains. Supportive
>management of life-threatening complications
>    from the infection, such as shock, hyperpyrexia, convulsions, and
>disseminated intravascular coagulation (DIC),
>    need to be initiated as they develop. 
>    d.  Prophylaxis. A formalin-killed Y. pestis vaccine is produced in the
>United States and has been extensively
>    used. Efficacy against flea-borne plague is inferred from population
>studies, but the utility of this vaccine against
>    aerosol challenge is unknown. Reactogenicity is moderately high and a
>measurable immune response is usually
>    attained after a 3-dose primary series: at 0, 1, and 4-7 months. To
>maintain immunity, boosters every 1-2 years
>    are required. Live-attenuated vaccines are available elsewhere but are
>highly reactogenic and without proven
>    efficacy against aerosol challenge. 
>Unsub info - send e-mail to majordomo@majordomo.pobox.com, with
>"unsubscribe liberty-and-justice" in the body (not the subject)
>Liberty-and-Justice list-owner is Mike Goldman <whig@pobox.com>

Paul Andrew Mitchell                 : Counselor at Law, federal witness
B.A., Political Science, UCLA;  M.S., Public Administration, U.C. Irvine

tel:     (520) 320-1514: machine; fax: (520) 320-1256: 24-hour/day-night
email:   [address in tool bar]       : using Eudora Pro 3.0.3 on 586 CPU
website: http://www.supremelaw.com   : visit the Supreme Law Library now
ship to: c/o 2509 N. Campbell, #1776 : this is free speech,  at its best
             Tucson, Arizona state   : state zone,  not the federal zone
             Postal Zone 85719/tdc   : USPS delays first class  w/o this

As agents of the Most High, we came here to establish justice.  We shall
not leave, until our mission is accomplished and justice reigns eternal.
[This text formatted on-screen in Courier 11, non-proportional spacing.]


Return to Table of Contents for

Supreme Law School:   E-mail