Active Ingredients: Ciprofloxacin
Macrophage disruption is mediated by an increase in the formation of Reactive Oxygen Species also known as Free Radicals. At high levels the toxins cause destruction of the macrophages.
At lower levels the toxin-mediated free radicals stimulates these cells to produce cytokines interleukin-1 beta and tumor necrosis factor-alpha, which induce systemic shock and death.
Antioxidants have been shown to moderately inhibit anthrax toxin-induced cytokine production in vitro.
The use of NAC prior to exposure to anthrax or its toxins have already been demonstrated to help reduce the negative effects of ROS and the release of cytokines in cell studies. NAC prior to exposure reduces the lethality of anthrax in animal studies.
Based on the findings of the animal and cell studies, glutathione and glutathione precursors containing cysteine or its physiologic form cystine represent a potent strategy for ameliorating the effects of inhalation anthrax.
Viruses are strands of information, either RNA or DNA, that depend on living cells to provide either the additional components or an environment which allow the virus to reproduce. Since they neither breathe nor reproduce on their own they are not considered living.
After using the host cell machinery and enzymes to make new copies of itself, viruses program the production of a new covering which allow it to be released out of the cell and accepted by the next cell.
To accomplish replication most viruses need to use the information contained in the DNA of the cell. Smallpox viruses are unusual in that they contain all of the information that they need to replicate, however it still needs the interior of the cell to replicate.
Smallpox virus, called variola, is a DNA virus containing all the information that is necessary to reproduce; however it must be incorporated into a cell for reproduction to occur.
This allows for the virus to replicate in the cytoplasm of a cell and to utilize the cell wall machinery to form a capsule and be released rapidly. The virus, after replicating in various tissue cells and creating a large number of copies, is released into the bloodstream before invading the skin and, in most cases, developing the skin lesions, or pocks that give rise to the common name for the disease state triggered by the virus: smallpox.
Usually 12 days after exposure a feverish illness appears. The rash appears as small pink spots called macules and progresses to enlarged, slightly raised papules.
The papules progress to blisters. Eventually the blisters become turbid, looking like pustules, which were previously called pocks and are the characteristic feature for which the virus is named. The pustules then dry up and shrink, leaving a hard crust that eventually flakes off leaving a sunken scar.
The distribution of the rash is characteristic of smallpox with the head and extremities affected more than the trunk. It is also possible to spread the virus without developing the rash, which means that outbreaks can be precipitated by individuals without rash or even severe illness.
Mortality: There is no treatment recognized once the illness has started. Poxviruses have caused infections in man documented as far back as the Egyptian pharaohs. The Pharaoh Ramses V was apparently inflicted with the virus at the time of his death in 1157 B.
Smallpox inflicted Europe in 710 A.