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) <snip> > >>From US ARMY HANDBOOK ON THE MEDICAL ASPECTS OF NBC DEFENSIVE OPERATIONS FM >8-9 >PART II - BIOLOGICAL, ANNEX B CLINICAL DATA SHEETS FOR SELECTED BIOLOGICAL >AGENTS >1 FEBRUARY 1996 >http://www.nbc-med.org/amedp6/PART_II/annexb.htm > >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 >therapy. > >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. 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