Once in the lymph nodes, the spores germinate into active bacilli that multiply and eventually burst the macrophages, releasing many more bacilli into the bloodstream to be transferred to the entire body. Once in the bloodstream, these bacilli release three proteins named lethal factor, edema factor, and protective antigen. The three are not toxic by themselves, but their combination is incredibly lethal to humans. Protective antigen combines with these other two factors to form lethal toxin and edema toxin, respectively. These toxins are the primary agents of tissue destruction, bleeding, and death of the host. If antibiotics are administered too late, even if the antibiotics eradicate the bacteria, some hosts still die of toxemia because the toxins produced by the bacilli remain in their systems at lethal dose levels. Exposure
The spores of anthrax are able to survive in harsh conditions for decades or even centuries. Such spores can be found on all continents, including Antarctica. Disturbed grave sites of infected animals have been known to cause infection after 70 years.Historically, inhalational anthrax was called woolsorters disease because it was an occupational hazard for people who sorted wool. Today, this form of infection is extremely rare in advanced nations, as almost no infected animals remain.Occupational exposure to infected animals or their products (such as skin, wool, and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common.
Swan neck deformity is a deformed position of the finger, in which the joint closest to the fingertip is permanently bent toward the palm while the nearest joint to the palm is bent away from it (DIP flexion with PIP hyperextension). It is commonly caused by injury, hypermobility or inflammatory conditions like rheumatoid arthritis or sometimes familial (congenital, like Ehlers–Danlos syndrome). Pathophysiology
Swan neck deformity has many of possible causes arising from the DIP, PIP, or even the MCP joints. In all cases, there is a stretching of the volar plate at the PIP joint to allow hyperextension, plus some damage to the attachment of the extensor tendon to the base of the distal phalanx that produces a hyperflexed mallet finger. Duck bill deformity is a similar condition affecting the thumb (which cannot have true swan neck deformity because it does not have enough joints). Diagnosis
Diagnosis of swan neck deformity is mainly clinical. MRI of the hand may suggest volar plate attenuation of PIP and extensor tendon damage for DIP  Genetic screening tests such as for CMT disease may also be indicated. Treatment
Splinting for fingers. Passive stretching and clearing the deformity. References
External links
Swan neck deformity at Wheeless Textbook of Orthopedics, a technical review of the condition
Rheumatoid arthritis: Image showing deformities