produces a capsule that is easily visualized using a methylene blue or India ink stain.
The anthrax toxin consists of three distinct antigenic components:
the oedema factor
, necessary for the oedema producing activity of the toxin;
the protective antigen
, which induces protective antibodies against the toxin and
the lethal factor
, essential for the lethal effects of the toxin.
is found in soil in many areas of the world.
The organism generally exists in the endospore form in nature.
Spores can persist in soil for decades.
Anthrax primarily is a disease of herbivores (eg, cattle, sheep, goats, pigs, bison, water buffalo, horses).
Anthrax in animals is hyperendemic or endemic in the following areas of the world:
Certain Southeast Asian countries (eg, Myanmar, Vietnam, Cambodia, Thailand)
In most of the rest of the world, anthrax occurs only sporadically.
Modes of Transmission
Illness in humans most commonly occurs following exposure to infected animals or contaminated animal
Contact with infected tissues of dead animals (eg, butchering, preparing contaminated meat), which
Consumption of contaminated undercooked meat, which can lead to gastrointestinal or
Contact with contaminated hair, wool, or hides (particularly during processing) or contact with
products made from them, which can lead to either inhalational or cutaneous anthrax.
Cases following laboratory exposure have been recognized.
Person-to-person transmission has not been recognized with gastrointestinal or inhalational disease.
Anthrax as a Bioterrorist Weapon. Weaponization for aerosol release generally involves:
Use of antimicrobial-resistant strains or genetic modification of the organism to increase
Pathogenesis of inhalational anthrax:
Endospores are introduced into the body via inhalation.
Endospores are phagocytosed by macrophages and carried to regional lymph nodes.
The endospores then germinate inside macrophages and become vegetative cells, which leave the
macrophages and multiply in the lymphatic system.
Bacteria enter the bloodstream and lead to septic shock and toxemia;
Regional hemorrhagic lymphadenitis of mediastinal and peribronchial lymph nodes causes the
occurrence of hemorrhagic mediastinitis.
Pulmonary lymphatic drainage can be blocked, leading to pulmonary edema.
Pleural effusions are common and may be massive.
Compression of the lungs and septic shock are the major causes of death.
The pathogenesis of cutaneous anthrax involves the following process:
Endospores are introduced through the skin (usually via preexisting skin lesions or abrasions).
Low-level germination at the site of introduction produces localized necrosis with eschar formation and
soft-tissue or mucosal edema (which can be massive in some cases).
Endospores often are phagocytosed by macrophages and carried to regional lymph nodes, causing
painful lymphadenopathy and lymphangitis.
Hematogenous spread with resultant toxemia can occur.
The pathogenesis of gastrointestinal anthrax.
Illness predominantly results from ingestion of large numbers of vegetative cells (such as may be found
in poorly cooked meat from infected animals).
Two forms of gastrointestinal anthrax have been recognized: oropharyngeal and gastrointestinal.
In oropharyngeal anthrax, a mucosal ulcer occurs initially, followed by regional lymphadenopathy and
In gastrointestinal anthrax, the portal of entry often is the terminal ileum or cecum. Intestinal lesions
occur and are followed by regional lymphadenopathy. Edema of the bowel wall and ascites (sometimes
Hematogenous spread with resultant toxemia can occur.
Incubation period 1-7 days (may be as long as 12 days) after skin exposure.
Patients complain of malaise and fever.
begins as a pruritic papule that enlarges
in 24-48 hours form an ulcer surrounded by a satellite vesicles filled with bloody or clear fluidand edematous halo
ulcer usually measures approximately 2-3 cm in diameter and has a round, regular, and raisededge.
ulcer characteristically is pruritic but not painful.
ulcer and surrounding edema evolve into a black eschar in 7-10 days
the membrane/exudate of the ulcer contains numerous anthrax bacilli
black eschar lasts for 12-14 days before separating and leaving a permanent scar.
The edema surrounding the ulcer may persist through the eschar stage.
of the nodes draining the infected area may occur
may persist long after disappearance of the ulcer/eschar.
Extensive nonpitting edema, lymphangitis, and painful lymphadenopathy may occur.
Currently most patients recover with appropriate antimicrobial therapy.
In preantibiotic era, case-fatality rates of about 20% were reported.
Two key features that distinguish cutaneous anthrax from other conditions in differential diagnosis are:
the relatively large extent of associated edema
Incubation period 1-7 days after exposure.
Patients complain of nausea, malaise, anorexia, which are accompanied by fever.
Patients with oropharyngeal anthrax may complain of unilateral sore throat/difficulty swallowing.
Oropharyngeal anthrax is the proximal GI manifestation of intestinal anthrax.
Mouth lesions may affect the hard palate or pharyngeal walls.
The anthrax ulcer in the oropharynx may be accompanied by a membrane and is associated withlocal edema and cervical adenopathy.
Death may result from asphyxiation due to neck edema or toxemia.
Patients with intestinal anthrax complain of nausea, vomiting, malaise, anorexia, severe abdominalpain, hematemesis, and bloody diarrhea, which are accompanied by fever.
Multiple anthrax ulcerative lesions are found throughout the GI tract secondary to hematogenousspread.
Primary intestinal anthrax has a local lesion resembling the ulcer of oropharyngeal anthrax.
Intestinal anthrax is difficult to recognize, and shock and death may occur 2-5 days after onset.
Case-fatality rate where patients received antibiotic therapy have ranged from 0% to 29%.
has been cultured from oropharyngeal swaps and stool specimens in patients with GIanthrax
Incubation period 1-60 days in weapon-grade anthrax
an initial prodrome (that includes symptoms such as low-grade fever, malaise, fatigue, anorexia,nonproductive cough, substernal discomfort)
followed by sudden increase in fever, diaphoresis, nausea or vomiting - hematemesis, severerespiratory distress, and chest pain, which may be so severe as to mimic an acute myocardialinfarction.and shock, if left untreated.
Inhalational anthrax presents as hemorrhagic mediastinitis. Abnormal chest radiograph:
~Mediastinal widening (70%)~Infiltrates, consolidation (70%)~Pleural effusion (80%)
Internal organs become darkly colored with widespread petechiae and hemorrhage.
Because humans are relatively resistant to invasion by B anthracis,
most cases of septicemicanthrax occur following inhalational anthrax.
May occur as complication of cutaneous, inhalational, or gastrointestinal anthrax and symptoms ofprimary site of infection usually will be present; however, meningitis may be the presenting illness.
Hemorrhagic meningoencephalitis is a characteristic presentation
Gram stain of CSF reveals many gram-positive rods
CT or MRI of head may show focal intracerebral hemorrhage, subarachnoid hemorrhage, diffusecerebral edema, intraventricular hemorrhage, and/or leptomeningeal enhancement.
Demonstration of B. anthracis
in a clinical specimen by microscopic examination of stained smears ofvesicular fluid, blood, cerebrospinal fluid, pleural fluid, stools, etc
Gram stain may reveal gram-positive rods; neutrophils are uncommon.
Histologic examination shows necrosis, edema, and lymphocytic infiltrate.
Isolation of B. anthracis
from a clinical specimen (e.g. blood, lesions, discharges). Culture on sheepblood or peptone agar.
Positive serology (ELISA, Western blot, toxin detection, chromatographic assay, fluorescent antibodytest (FAT)). Test is positive if a single acute-phase titer is highly elevated or if a 4-fold greater rise inthe titer is observed between acute and convalescent specimens.
are used for the treatment of anthrax. Intravenous administration is
recommended in cases of inhalational, gastrointestinal, meningeal anthrax and cutaneous anthrax with
signs of systemic involvement.
had a synergistic effect with penicillin in experiments and may also be given for
Despite early and vigorous treatment, the prognosis of patients with inhalational, gastrointestinal, ormeningeal anthrax remains poor.
Chloramphenicol, erythromycin, tetracycline, or ciprofloxacin
can be administered to patients who
are allergic to penicillin.
Clindamycin may be added
for its anti-exotoxin effect.
Ampicillin (meningeal doses), doxycycline, and chloramphenicol penetrate the CSF, which is important inmeningeal anthrax.
Antibiotic therapy should be continued for at least 14 days after symptoms abate
for bioterrorist anthrax to prevent inhalation anthrax should be continued for 60
days due to the danger of delayed spore germination.
Use amoxicillin, doxycycline, or any quinolone
(eg, ciprofloxacin, levofloxacin, gatifloxacin) for
postexposure prophylaxis to prevent inhalation anthrax.
Other antibiotics that may be useful include erythromycin, first-generation cephalosporins,chloramphenicol, clindamycin, vancomycin, carbapenems, cefoperazone, and extended-spectrumpenicillins or trimethoprim-sulfamethoxazole (TMP-SMX).
No reason exists for instituting double-drug coverage against B anthracis,
which is a very sensitiveorganism.
The availability of anthrax vaccine is limited to military personnel.
Patients with cutaneous anthrax have a persistent circular scar at the point of eschar formation.
Patients with inhalational, oropharyngeal, or cutaneous (neck) anthrax may develop an airwayobstruction.
Patients with septicemic anthrax may develop overwhelming toxicity or shock.
Patients with inhalational anthrax also often develop hemorrhagic leptomeningitis.
If treated early, patients with cutaneous anthrax have a good prognosis.
Patients with inhalational anthrax have the worst prognosis.
The prognosis for patients with oropharyngeal or intestinal anthrax is not as favorable as the prognosisfor patients with cutaneous anthrax but is more favorable than for patients with inhalational anthrax.
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