• Ames strain (isolated from a dead Texan cow in 1981)
• Florida strain (used as a bioweapon in 2001, differing from Ames strain only in 11 bp out of 5,000,000 (5,000 genes))
• Sterne strain is an avirulent, nonencapsulated strain that produces sublethal amounts of the toxin inducing formation of protective antibody (used for subunit vaccine)

Epidemiology :

• hyperendemic in Tamil Nadu, India
• west and north China
• anthrax has been a problem in Masvingo, Zimbabwe, since it was first reported there in 2000; in that year 1182 people were reported affected in Zimbabwe with 11 deaths. With the increasing and widespread rural poverty in Zimbabwe, instructing the local population not to eat sick and dead stock is at best wishful thinking. This now seems to be a replay of the human epidemic in 1972-80, when some 10 000 people were afflicted with anthrax. When the country had an effective veterinary service, this disease was of trivial importance. Because of the traditional social and cultural aspects of the country, the disease has a human impact out of proportion to the numbers of cattle affected. Anthrax outbreaks in Zambia in the west and eastern provinces of the country are of different genetic strains : outbreaks have occurred intermittently in Mongu for some time. Zambia, India, Russia, and countries in Central Asia take a reactive posture to anthrax and initiate vaccination only when either human or livestock cases are reported. Sterne and its Russian equivalents are some of the cheapest vaccines available for any disease, human or animal; in North America Sterne costs 40 cents/dose.
• Indonesia : endemic in several provinces, including West Java, Central Java, Yogyakarta, South Sulawesi, Central Sulawesi, Southeast Sulawesi, and East Nusa Tenggara. Sporadic outbreaks occurred in 2001.
• USA, only 235 cases were reported between 1955 and 1994, with 11 cases inhalational. On early October 2001, anthrax spore came mixed in a

white powder by mail to the 3-story building of the old American Media Inc.. Bob Stevens, an AMI photo editor, was killed and 17 others were made sick. The contamination was throughout the building. The only way it could be explained was that when the janitorial team came in following the opening of the spore bearing envelope(s) (there is a suspicion that there might have been more than one), the vacuum cleaners just energized the spilt spores, and the internal ventilation system did the rest, which just goes to show that host factors play an important part in selecting who gets infected or not. Fortunately, with few exceptions, it was "not". Decontamination was performed by Bio-ONE and checked by Marcor Remediation Inc in 2006^ref. At least 7 people in an Oakland, Calif., research laboratory have been inadvertently exposed to live anthrax bacteria that had twice been tested to be dead, once by the vendor company (Southern Research Institute (SRI), Frederick, Md.) that shipped the sealed liquid agent via FedEx, double-boxed, on March 2004 and once in the lab. The 7 work at Children's Hospital and Research Center at Oakland in a BSL-2 facility located 1 mile from the hospital, and no one at the hospital itself was exposed. 3 researchers (a lead researcher, 2 lab technicians and an animal handler) were trying to develop antibodies to the spore exosporium using Bacillus anthracis (Michelle Mock at the Pasteur Institute, Paris, has nicely shown that if you mix dead spores with PA you get enhanced immunity. Sterne vaccine is pathogenic for mice at certain doses but can be used safely at lower doses. Plus it is available and certainly cheaper than whatever they got from SRI, which might well have been intended to be dead Sterne anyway)that had supposedly been heat inactivated, while the other 4 people, and perhaps a few others yet to be determined, worked in the lab but not on the project : all 7 have been put on a 60-day regimen of ciprofloxacin. They injected mice on 28 May 2004 and over that weekend, 10 mice died in separate cages, and animal handlers placed the mice in a freezer. It was not brought to the immediate attention of lead researchers that all the mice in the 1st experiment had died. Last Friday, another batch of mice was inoculated with the deadly agent. On Monday, those mice, too, were dead, and the lead researcher obtained cultures from the cavity of a dead mouse. By Wednesday, the researchers discovered the anthrax organism growing in the abdominal cavity of the dead mouse. 49 of 50 mice inoculated with the B. anthracis quickly died. Subsequent attempts to culture both the material and a sample from one of the dead mice both showed the bacteria was alive. The Federal Bureau of Investigation removed the remaining material from the lab on June 9 night. Researchers had been wearing masks and proper clothing, and the lab's air is filtered both entering and leaving. The sample sent to the Oakland lab is the only heat-inactivated B. anthracis sample SRI has ever shipped to any lab, and the SRI material is a heat-resistant mutant strain of B. anthracis. Although both SRI and the Oakland lab cultured the shipment of B. anthracis, the Oakland lab did not subculture it by taking a sample of the first culture and transferring it to a fresh culture dish. Voss said he doubts SRI subcultured it either, although he has not yet verified that fact. With some bacteria, subculturing is important because it won't grow otherwise. Before the letters of 2001 there were probably only about a dozen US institutes working with B. anthracis; now apparently there are 350. On 16 Feb 2006, a 44 year old male was diagnosed in a hospital in Pennsylvania with inhalation anthrax, confirmed by CDC, but he is doing well. 4 other individuals apparently exposed to the same untreated animal hides are being evaluated, and the 3 evaluated so far (one is in transit) are well and are receiving antimicrobial prophylaxis. Patient resides in New York City and makes drums from unprocessed domestic and imported (Africa) animal hides (cow and goat). Patient reports frequent travel to Africa (most recent travel 4 & 21 Dec 2005). Patient reports last work with animal hides on 15 Feb 2006. Process includes cleaning and removal of hair from hides without chemical fixatives. While traveling to Pennsylvania on 16 Feb 2006, the patient collapsed with rigors and was transported and admitted to a small local hospital^ref.
• Turkey : anthrax is probably hyperenzootic, with the number of human cases reported annually in the >300 cases/year range: 1999 (690 cases); 2000 (396); 2001 (532); 2002 (368); & 2003 -- last year of available data -- (325). When there are human cases of anthrax it is because the veterinarians have failed. There is a strange blindness by livestock owners to disregard deaths in sheep and goats. All too often I have heard accounts of ovine or caprine flock deaths having to reach 100 before a diagnosis is sought and control procedures are implemented. I suspect it is because cattle are kept by men and community leaders, and sheep and goats are looked after by women and marginal groups. This is a bit of an over-statement to make the point, but ignoring small ruminant health problems occurs far too often. While the unit value of cattle is high and therefore the loss of one animal is significant, families and communities depend on sheep and goats for food, protein, wool and hair. Therefore their health may be affected more by the latter animals' health than by that of cattle.
• Russia : During 1999-2004 in Russia 155 cases of anthrax were registered in humans, including  16 in 2004. All had taken part in the slaughter of cattle, butchering carcasses, and/or the transportation of meat. Regarding anthrax in animals, in 2004, 3 outbreaks occurred in Russia with a total of 9 animals affected. In 2003 there were 11 outbreaks and 18 animals affected. In Russia there are unreported cases, and frequently cattle are not vaccinated prophylactically, which maintains the threat of disease. In 2003, 125 048 persons were vaccinated against anthrax; in 2004, 114 390. The widespread anthrax in Russia in the past and the repeated annual outbreaks mean that there is a constant threat of anthrax in animals and people.  The above data are taken from the state report "About sanitary and epidemiological situation in the Russian Federation in 2004"^ref. There is, unfortunately, a long tradition of vaccinating humans against anthrax in Russia. These annual figures starkly underline the failure of the Russian veterinary services in controlling this disease, even if one were to claim that the risk of infection is sometimes applied with a broad public health brush. Unless one is dealing with occupational industrial exposure to infected hides or contaminated wool or hair, any human case of anthrax and any need to vaccinate humans (outside of research laboratories) reflects a failure of the veterinary profession wherever such a situation exists
• Italy :
• Year / Human cases / Bovine outbreaks / Bovine cases / Caprine outbreaks / Caprine cases
• 1985 / 37
• 1986 / 29
• 1987 / 9
• 1988 / 12 / 7 / 26 / 11 / 246
• 1989 / 11 / 12 / 29 / 5 / 6
• 1990 / 14 / 5 / 7 / 11 / 47
• 1991 / 9 / 7 / 23 / 9 / 146
• 1992 / 0 / 3 / -- / 4 / 11
• 1993 / 0 / 20
• 1994 / 0 / 2 / 2 / 8 / 70
• 1995 / 0 / 1 / 1 / 1 / 1
• 1996 / 0 / 13 / 46 (included 12 outbreaks of bovine anthrax in Sardinia)
• 1997 / 1 / 4 / 4 / 11 / 44 (outbreaks of bovine anthrax in Basilicata, Lazio, Sicily, Campanna, Sardinia, Calabria and Puglia)
• 1998 / 1 / 9 / 14 / 3 / 3 (outbreaks of bovine anthrax in Calabria, Basilicata, Umbria,  and Veneto regions)
• 1999 / 0 / 3 / 3 / 3 / 5
• 2000 / 0 / 2 / 2 / 6 / 13
• 2001 / 0 / 1 / 1 / 2 / 8
• 2002 / 0
• 2003 / 0
• 2004 / -- / -- / 54 / -- / 11 (outbreaks of bovine anthrax in Basilicata)
One outbreak of swine anthrax (1 case) was reported in 1990; 0 in 1997; 1 (in Basilicata) in 2004. 4 infected red deer were reported in Basilicata during 2004. Notable outbreaks:
• 1975 to 1977 - Outbreaks in Milan were associated with processing imported animal hides from Africa^ref
• 1992 (publication year) - An outbreak (3 cases) of cutaneous anthrax among members of a family was associated with an infected cow^ref
• UK : the last known human death was in 1974
• Scotland : 1 case in 1987 (a young girl who later recovered) and 1 case in 2006 (a 50-year-old man at Black Lodge in Stobs, Hawick, who died in July^{ref1, ref2, ref3}). The most recent scare was at a farm in Lennoxtown, East Dunbartonshire, where a cow was suspected to have died from the disease in 2002, but hadn't.
• Wales : in 2002, when a cow died at a farm in Wrexham, north Wales; on 19 April 2006 Ynys Gau farm, at Gwaelod-y-Garth, near Cardiff, was closed off to the public when the animals suddenly died. No humans were infected, and the farm was eventually reopened 20 days later after being given the all-clear from government vets
• Romania regularly reports a few cases in cattle and sheep each year, and occasionally in horses and swine. Human cases reflect this: 2000 (51 with 2 deaths); 2001 (7); 2002 (1); 2004 (2); and 2005 (1)
• Kazakhstan : > 300 natural foci of anthrax exist in Southern country. Some 3-4 years ago about 20 cases of anthrax were registered annually in the region. In 2005 a preliminary diagnosis of anthrax was reported in 4 inhabitants of Southern Kazakhstan.
• Indonesia : anthrax is sporadic through much of the country now having once been under good control, affecting cattle, small ruminants, buffalo, and occasionally horses and pigs. It is seen on West Sumatra, Jambi, DKI Jakarta, West Java, Central Java, West Nusa Tenggara, East Nusa Tenggara, South Sulawesi, Southeast Sulawesi, & Central Sulawesi

• capsule (only in S colonies), which is made up of...
• capsular polypeptide (poly(D-Glu)) : catalyzing enzyme is coded by pXO2 plasmid.
• a polysaccharide cross-reacting with human RBCs
• a common protein.
It can be detected by the Loeffler's stain or McFadyean reaction.
• anthrax toxin, whose components are coded by pXO1 plasmid :
• A subunits :
• p89^{factor I / oedema factor (OF) / edema factor (EF)} is a Ca²⁺₄CaM-dependent adenylate cyclase similar to the Bordetella pertussis adenylate cyclase toxin. As no CaM exists in prokaryotes, the toxin is only active in the eukaryotic cell.
• p83^{factor II / protective antigen (PA)} / PA83, so named as it induces protective antitoxic antibodies in guinea pigs
• B subunit : p90^{factor III / lethal factor (LF)} is a Zn²⁺-dependent protease that cleaves and inactivates ...
• MEK1 and MEK2 => inhibition of p38^MAPK1 activation (which synergize with NF-kB to induce the expression of antiapoptotic genes in macrophages) => apoptosis of macrophages and prevents maturation of DCs, so enabling the bacterium to evade the innate immune response : T cells are activated initially but fail to differentiate into memory cells.
• MEK6 / MKK6 => inhibition of IRF3 pathway => impaired proinflammatory cytogine gene expression^ref.
LF is neutralized by a-defensin 1
p83^PA binds to vWF A domain in anthrax toxin receptor (ATR, an ubiquitary type I transmembrane protein => pantropic toxin) : then it is cleaved in the tetrabasic RKKR¹⁶⁷ site by subtilisin-like proteases belonging to the furin family (furin, PC1 / SPC3, PC2, ..) and loses a p20 fragment. The p63 fragment (PA63) remains bound to ATR and oligomerizes to form (ATR-PA63)₇, to which both EF and LF bind : ATR clustering causes association with lipid raft and clathrin-mediated RME : in late endosomes, pH lowering allows p63 homoheptamer to create a functional pore that lets EF and LF escape into the cytosol and reach their targets. During conversion of the heptameric precursor to the pore, the 7 Phe⁴²⁷ residues converged within the lumen, generating a radially symmetric heptad of solvent-exposed aromatic rings. This "j-clamp" structure was required for protein translocation and comprised the major conductance-blocking site for hydrophobic drugs and model cations. The j-clamp serves a chaperone-like function, interacting with hydrophobic sequences presented by the protein substrate as it unfolds during translocation^ref.
Lethal toxin (LT) is a complex of activated PA and LF.

• infected Ovis aries, Bos taurus, Sus scrofa, Odocoileus virginianus, Tragelaphus strepsiceros, and Equus caballus and their derivatives. Birds are normally resistant to this infection. the disease is rarely seen in calves. While some textbooks describe B. anthracis germinating in wet, warm soils, there is very little evidence that this does occur outside the laboratory. This has only been achieved in the laboratory and with sterile soil. See Minette & Dhanda 1944 -- present-day researcher claims notwithstanding.  In Russia, they had an initial growth but only after adding blood to the soil, i.e. excess nutrients. And any vegetative B. anthracis cells would not survive passage through the ruminant stomach and abomasum. It is more certain that these outbreaks occur through the ingestion of spores surviving from buried previous cases, where there had been ample opportunity for sporulation, either because the animal carcass had been necropsied or had been opened up by scavengers. Guidelines for animal outbreaks :
• move the animals away from the area of maximum risk, e.g., where the carcasses are and where the original source may have been, and dispose of the carcasses by burning (neither cut open nor burial as skinned and butchered carcasses are certain to have a plenitude of spores that will rise from the grave to cause problems another day)
• treat the herd, or at least all those animals that are at patent risk of the disease, with LA200 or any other long-acting penicillin/antibiotic. This will stop any incubating infections; if you depend solely on vaccination it can take 8 days while deaths continue before there is any significant immune protection. (Because LA200 stings badly, it is better to treat horses BID with an injectable penicillin for 3 days. If LA200 is used on horses, they won't let you near them when you later have to vaccinate them, or if they do you may end up spending some days in hospital.)
• wait 7-10 days for the antibiotic to clear from their systems
• vaccinate the whole herd with Sterne vaccine. The STI and Sterne vaccines are normally very efficient at protecting livestock. The usual "failures" of vaccination occur when animals already incubating the disease are vaccinated, or when animals are receiving antibiotics at the time they are vaccinated. People forget that antibiotics inserted up the teat to control mastitis will interfere with this live vaccine. Universal experience is that anthrax deaths stop in a herd by 8 days after vaccination thanks to the immunity provided and in spite of any continuing exposure.
• repeat annual herd vaccinations with Sterne for at least 3 more years. Farmer failure to vaccinate in the spring ahead of the anthrax 'season' is a global problem -- it is a common cause of outbreaks in Alberta and Saskatchewan, Canada, for example
While animals can be safely moved to another farm or ranch by 14 days after vaccination, animals going to slaughter after being given antibiotics should be held back longer. This period is variably defined and depends entirely on local regulations. The vaccine site can be trimmed out by the meat inspector, though some remove the whole quarter.
• there are rare case reports of person-to-person transmission of cutaneous disease.
• bioweapons

contact in skin injuries (95% : typically on the exposed skin areas such as the arms, hands, face and neck) => cutaneous anthrax^ref (hemorrhagic angioflogosis) after 2-5 days incubation : gelly oedema =12-36 hrs.=> bite-appearing, painless, pruritic papule that enlarges and erodes => ulcer (Siberian ulcer) surrounded sometimes by vesicles, painful locoregional lymphadenitis, and fever => pustule (malignant pustule) => 1-3 cm black eschar that is painless with surrounding prominent edema at day 7-8 => self-limiting local infection : 20% evolve to septicemia => meningitis (5%) => coma vigil / "typhoid status". Regional lymphadenitis may also occur within 7 days. If on neck malignant oedema may lead to tracheal compression. Specific antimicrobial therapy does not seem to alter the natural progression of the local lesion but does assist in minimizing systemic symptoms and/or bacteraemic spread. Differential diagnosis of eschar and ulceration^{ref1, ref2} : a common initial diagnosis is that of a pruritic and papular arthropod bite in the majority of patients. Once an ulcer or eschar develops, the differential diagnosis includes:
• antiphospholipid antibody syndrome ulcers
• aspergillosis
• brown recluse (Loxosceles reclusa) spider bite, also in Africa. A 7-month-old male infant was hospitalized on 2001 in New York with a presumptive diagnosis of necrotic arachnidism with superimposed cellulitis, but after anthrax exposure was reported at another television network, 2 punch biopsies of the lesion were performed and PCR and immunostaining were positive^ref
• coumadin necrosis
• ecthyma gangrenosum
• factitial ulcer
• glanders
• heparin necrosis
• cutaneus leishmaniasis
• mucormycosis
• orf/milker's nodule
• plague
• rat bite fever
• rickettsial pox
• staphylococcal/streptococcal ecthyma
• tropical ulcer
• tularemia
• scrub typhus
• tick typhus
Historically, the case-fatality rate for cutaneous anthrax has been < 1% with antibiotic treatment and 20% without antibiotic treatment.
Cutaneous anthrax in Lima, Peru: retrospective analysis of 71 cases, including 4 with a meningoencephalic complication^ref. Human cutaneous cases directly from contaminated soil are frankly rare. The more usual backstory to such claimed events is that the affected person was involved in butchering a sick animal; for fear of the legal repercussions of failing reporting that the animal was sick and selling said meat in a local market, the true events get covered up. There is a steady pitter-patter of sporadic anthrax outbreaks and cases in Romania in spite of some 3.5 million cattle and over 9 million sheep and goats being vaccinated each year. Their control programme needs a critical re-examination to determine why it is not more cost-effective. Human cutaneous anthrax cases carry a 10% risk of lethality, especially if treatment is delayed or missed; prompt early treatment with appropriate antibiotics is virtually 100% successful. However, once a systemic infection has set in, death is almost inevitable in humans.
inhalation of intentional or unintentional aerosolized spore aggregates with Ø < 5 mm (the bacterial spores usually clump together and hard to suspend in the air : to make them a deadly weapon, they have to be separated and combined with fine dust particles to increase the time of floating in the air) => pulmonary or inhalational anthrax / wool sorters' disease after 1-5 days incubation (however, due to spore dormancy and slow clearance from the lungs, the incubation period for inhalational anthrax may be prolonged to > 2 weeks) : phagocytated by alveolar macrophages => prodrome of high fever with chills, cough (first non-productive, then hemoptysis), chest pain, headache, myalgias, and malaise => respiratory failure (tachypnea and tachycardia), nausea and vomiting, systemic arterial hypotension, mild or severe leukocytosis, thrombocytopenia, mediastinic lymphadenitis with hemorrhagic necrosis => hemothorax. Widened mediastinum is the classic finding on imaging of the chest, but may initially be subtle^ref : 5% undergo septicemia => meningoencephalitis=> coma vigil / "typhoid status". Survival after symptoms have started can be rare. Case-fatality rates for inhalational anthrax are high, even with appropriate antibiotics, and supportive care. Following the bioterrorist attack in Autumn 2001, the case-fatality rate among patients with inhalational disease was 45% (5/11). Person-to person spread of inhalational anthrax has not been documented.
ingestion of unproperly cooked meat or milk from an infected herbivore  =>
• oro-pharyngeal anthrax
• gastro-intestinal or enteric anthrax : penetration into mucosa through a preexisting lesion => phagocytosed by macrophages => hemorrhagic mesenteric lymphadenitis => after 2-5 days incubation : fever, abdominal pain, nausea and vomiting, bloody  diarrhea, perforation (=> peritonitis) or septicemia (=> meningoencephalitis => coma vigil / "typhoid status"). Lethality : 25-50%.
Populations who regularly eat anthrax-infected carcasses have a moderate prevalence of antibodies, which, unfortunately or fortunately -- depending on how one interprets the data -- is believed to suppress the incidence of clinical intestinal anthrax and thereby provides an excuse to those communities to continue to eat meat from a sick cow (in West Bengal this a common practice in all tribal areas as well as in poor communities)

• PCR : single nucleotide polymorphisms (SNPs) are increasingly recognized as important diagnostic markers for the detection and differentiation of Bacillus anthracis. The use of SNP markers for identifying B. anthracis DNA in environmental samples containing genetically similar bacteria (B.cereus and B.thuringiensis) requires the ability to amplify and detect DNA with single nucleotide specificity. A TaqMan^® mismatch amplification mutation assay (TaqMAMA) around a SNP in the plcR gene of B. anthracis permits specific, low-level detection (25fg DNA) of this B. anthracis-specific SNP, even in the presence of environmental DNA extracts containing a 20,000-fold excess of the alternate allele. The ability to selectively amplify and detect low copy number DNAs with single nucleotide specificity will represent a valuable tool in the arena of biodefense and microbial forensics^ref
• fixed and stained (even if only with Gram's stain) smear and culturing of CSF, blood and pleural exudate; heat-stable Ags may be precipitated by immune sera (Ascoli thermoprecipitation). It is difficult to detect the organism in human cutaneous lesions, and by 13 days post-infection, impossible

• antibacterials (ciprofloxacin, levofloxacin, clindamycin, rifampin, penicillin and tetracyclines). The decision regarding the use of penicillins, the drugs historically used for treatment and prophylaxis of anthrax, is complicated. An inhibition assay shows beta-lactamase activity at low levels in the isolates. Genomic sequence data show 2 b-lactamases: a potential penicillinase (class A) and a cephalosporinase (class B), which is expressed. Concern about the use of penicillin arises because an inducible penicillinase could be activated in the face of treatment with b-lactams, particularly if the number of organisms present is high, as appears typical with inhalational disease. Concerns have also been raised about the poor penetration of b-lactams into macrophages, the site where B. anthracis spores germinate. At present the recommendations are for use of the ciprofloxacin or doxycycline with the caution that the latter should not be used if meningitis is suspected as central nervous system penetration is insufficient for treatment purposes.  A multidrug regimen is suggested when bacteremia is present, using either ciprofloxacin or doxycycline along with one or more agents to which the organism is typically sensitive
• protocol for cutaneous anthrax^ref :
• adults : ciprofloxacin 500 mg BID or doxycyclin 100 mg BID for 60 days
• children : ciprofloxacin 10-15 mg/kg/day every 12 hours (not to exceed 1 g/day) or doxycyclin (<= 8 years : 2.2 mg/kg every 12 hours; > 8 yrs and < 45 kg : 2.2 mg/kg every 12 hrs; > 8 yrs and > 45 kg : 100 mg every 12 hrs) for 60 days
• pregnant women : ciprofloxacin 500 mg BID or doxycycline 100 mg BID for 60 days
• immunocompromised persons : same for nonimmunocompromised persons and children
Cutaneous anthrax with signs of systemic involvement , extensive edema, or lesions on the head and neck require intravenous therapy, and a multidrug approach is recommended. Ciprofloxacin and doxycycline should be considered first-line therapy. Amoxicillin 500 mg po TID for adults of 80 mg/kg/day divided every 8 hours for children is an option for completion of therapy after clinical improvement. Oral amoxicillin dose is based on the need to achieve appropriate minimum inhibitory concentration levels. Previous guidelines have suggested treating cutaneous anthrax for 7-10 days, but 60 days is recommended in the setting of a bioterror attack, given the likelihood of exposure to aerosolized B.anthracis. The American Academy of Pediatrics recommends treatment of young children with tetracyclines for serious infections (e.g. Rocky Mountain spotted fever). Although tetracyclines or ciprofloxacin are not recommended during pregnancy, their use may be indicated for life-threatening illness. Adverse effects on developing teeth and bones are dose-related; therefore, doxycycline might be used for a short time (7-14 days) before 6 months of gestation.
• protocol for oropharyngeal, gastrointestinal and inhalational anthrax^ref :
• adults : ciprofloxacin 400 mg every 12 hours or doxycycline 100 mg every 12 hours and 1 or 2 additional antimicrobials. IV treatment initially Switch to oral antimicrobial therapy when clinically appropriate : ciprofloxacin 500 mg po BID or doxycycline 100 mg po BID. Continue for 60 days (IV and po combined).
• children : ciprofloxacin 10-15 mg/kg every 12 hours or doxycycline (> 8 years and >= 45 kg : 100 mg every 12 hrs; > 8 years and <= 45 kg : 2.2 mg/kg every 12 hrs; <= 8 yrs : 2.2 mg/kg every 12 hours) and 1 or 2 additional antimicrobials. IV treatment initially Switch to oral antimicrobial therapy when clinically appropriate : ciprofloxacin 10-15 mg/kg/day po every 12 hours or doxycycline (> 8 years and > 45 kg : 100 mg po BID; > 8 years and <= 45 kg : 2.2 mg/kg po BID; <= 8 yrs : 2.2 mg/kg po BID). Continue for 60 days (IV and po combined).
• pregnant women : same for nonpregnant adults (the high death rate from the infection outweighs the risk posed by the antimicrobial agent).
• immunocompromised persons : same for nonimmunocompromised persons and children
Ciprofloxacin and doxycycline should be considered an essential part of first-line therapy for inhalational anthrax. Steroids may be considered as an adjunct therapy for patients with severe edema and for meningitis based on experience with bacterial meningitis of other etiologies. Other agents with in vitro activity include rifampin, vancomycin, penicillin, ampicillin, chloramphenicol, imipenem, clindamycin, and clarithromycin. Because of concerns of constitutive and inducible b-lactamases in Bacillus anthracis, penicillin and ampicillin should not be used alone. Consultation with an infectious disease specialist is advised. Initial therapy may be altered based on clinical courses of the patient : 1 or 2 antimicrobial agents (e.g. ciprofloxacin or doxycycline) may be adequate as the patient improves. If meningitis is suspected, doxycycline may be less optimal because of poor CNS penetration. Because of the potential persistence of spores after an aerosol exposure, antimicrobial therapy should be continued for 60 days. If intravenous ciprofloxacin is not available, oral ciprofloxacin may be acceptably because it is rapidly and well absorbed from the gastrointestinal tract with no substantial loss by first-pass metabolism. Maximum serum concentrations are attained 1-2 hours after oral dosing but may not be achieved if vomiting or ileus are present. In children, ciprofloxacin dosage should not exceed 1 g/day. The American Academy of Pediatrics recommends treatment of young children with tetracyclines for serious infections (e.g. Rocky Mountain spotted fever). Although tetracyclines or ciprofloxacin are not recommended during pregnancy, their use may be indicated for life-threatening illness. Adverse effects on developing teeth and bones are dose-related; therefore, doxycycline might be used for a short time (7-14 days) before 6 months of gestation.
• LF inhibitors do not affect the prototype human MMP that are structurally similar to LF. Initial in vivo evaluation of postexposure efficacy of these inhibitors combined with antibiotic ciprofloxican against B. anthracis resulted in significant protection^ref.
• anti-PA mAbs

animal model	ID50	LD50	[bacteria]blood at death
Mus musculus	5 cells	1,000 units/kg	107 / mL
Macaca mulatta	3,000 cells	2,500 unit/kg	107 / mL
Rattus norvegicus	106 cells	15 units/kg	105 / mL

• WHO Anthrax Guide
• World Anthrax Data Site
• Grid-computing : anthrax research

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