78. Gold H. Treatment of anthrax. ;26:-

The current understanding that anthrax is a toxigenic condition suggests the potential of antitoxin therapy. The central importance of lethal toxin is supported by much research. Early experiments in which antibiotics were administered to animals at different stages of infection found a principle of “no return”; once the infection had reached a certain point, the animal was doomed, even after removal of the microbes. Test animals injected intravenously with purified lethal toxin died in a manner very similar to that of animals that died of the natural infection. Lethal-toxin–deficient strains are highly attenuated. Prior immunity (passive or active) to the lethal-toxin proteins protects animals from endospore challenge. Finally, toxin-affected macrophages produce the proinflammatory cytokines that mediate the shock and sudden death that occur in anthrax. Unfortunately, antitoxin preparations are not currently available in the United States. In addition, the recent discovery that lethal toxin acts as a zinc metalloprotease inside target cells and the identification of potential target substrates may provide new insights for use in designing drugs that directly inhibit the toxicity of lethal factor in vivo.

19/10/2001 · The 2001 anthrax attacks in the ..

103. Shlyakhov EN, Rubinstein E. Human live anthrax vaccine in the former USSR.  ;12:-

2001 anthrax attacks - Wikipedia

Oropharyngeal anthrax is less common than the gastrointestinal form. It is also associated with the ingestion of contaminated meat. Initial symptoms include cervical edema and local lymphadenopathy, which cause dysphagia and respiratory difficulties. Lesions can be seen in the oropharynx and usually have the appearance of pseudomembranous ulcerations. This form is milder than the classic gastrointestinal disease and has a more favorable prognosis.

Anthrax is a virulent, contagious, and potentially fatal disease

Inhalational anthrax is usually fatal, even with aggressive antimicrobial therapy. It appears that only about one fifth of those who contracted inhalational anthrax in Sverdlovsk recovered. Anthrax spores are about 1 to 2 μm in diameter, a size that is optimal for inhalation and deposition in the alveolar spaces. Although the lung is the initial site of contact, inhalational anthrax is not considered a true pneumonia. In most but not all cases, there is no infection in the lungs. Rather, the endospores are engulfed by alveolar macrophages and transported by them to the mediastinal and peribronchial lymph nodes, with the spores germinating en route. Anthrax bacilli multiply in the lymph nodes, causing hemorrhagic mediastinitis, and spread throughout the body in the blood.

119. Knudson GB. Treatment of anthrax in man: history and current concepts.  ;151:-
81. Shlyakhov E, Rubinstein E. Evaluation of the anthraxin skin test for diagnosis of acute and past human anthrax.  ;15:-

Last Word Archive | New Scientist

summarizes pharmacologic therapy for anthrax. Penicillin and doxycycline are used for the treatment of anthrax. Intravenous administration is recommended in cases of inhalational, gastrointestinal, and meningeal anthrax. Cutaneous anthrax with signs of systemic involvement, extensive edema, or lesions on the head and neck also requires intravenous therapy. Streptomycin had a synergistic effect with penicillin in experiments and may also be given for inhalational anthrax. Despite early and vigorous treatment, the prognosis of patients with inhalational, gastrointestinal, or meningeal anthrax remains poor. Antibiotic therapy should be continued for at least 14 days after symptoms abate. In cutaneous anthrax, treatment with oral penicillin renders lesions sterile after 24 hours, although they still progress to eschar formation. Chloramphenicol, erythromycin, tetracycline, or ciprofloxacin can be administered to patients who are allergic to penicillin. If resistance to penicillin and doxycycline is suspected and antibiotic-susceptibility data are not available, ciprofloxacin may be administered empirically. Doxycycline and tetracycline are not recommended for pregnant women or children, and the effects of ciprofloxacin in pregnant women have not been determined.

(11 AM Micro) found an article which discusses the treatment for severe cases of anthrax

The ecology of Bacillus anthracis - ScienceDirect

The smaller capsule-bearing plasmid, pXO2, is 95.3 kbp in size and codes for three genes (and ) involved in the synthesis of the polyglutamyl capsule. The exotoxins are thought to inhibit the immune response mounted against infection, whereas the capsule inhibits phagocytosis of vegetative anthrax bacilli. The expression of all known major virulence factors is regulated by host-specific factors such as elevated temperature (≥37°C) and carbon dioxide concentration (≥5 percent), and by the presence of serum components. Regulation of the expression of the toxin and capsule genes is mediated by the transcriptional activator AtxA, whose activity appears to be affected by the previously mentioned environmental conditions. Expression of the capsule gene is also controlled by its own transcriptional regulator, AcpA. Both plasmids are required for full virulence; the loss of either one results in an attenuated strain. Historically, bacterial strains for anthrax vaccine were made by rendering virulent strains free of one or both plasmids. Pasteur, an avirulent pXO2-carrying strain, is encapsulated but does not express exotoxin components. Sterne, an attenuated strain that carries pXO1, can synthesize exotoxin components but does not have a capsule.

A media report released Wednesday, Dec

Panel A shows the characteristic blackened eschar surrounded by eroded areas and massive edema. These lesions are painless. The areas of “dried skin” represent resolving edema. Lesions continue to progress despite rigorous antibiotic treatment. Cutaneous anthrax can be self-limiting, and the lesions resolve without scarring. About 10 percent of untreated cutaneous anthrax infections progress to systemic anthrax. Panels B, C, and D show changes in the lesion on the cheek over a seven-day period. The characteristic blackened eschar is present on day 0 (Panel B). Facial edema and ulceration occur by the second day (Panel C). On day 7, the lesion is beginning to heal, and the facial edema is resolving (Panel D). The photograph in Panel A was kindly provided by Drs. Wilhelm Kobuch and P.C.B. Turnbull. The photographs in Panels B, C, and D are reprinted from Smego et al. with the permission of the publisher.