Anthrax threat: a review of clinical and diagnostic measures.
ABSTRACT Anthrax is the plague of the ancient world and its existence is confirmed by the Roman poet Virgil. Also it is a threat in the modern world as it can be used in biological wars and bioterrorism. Anthrax is caused by Bacillus anthracis an unmovable, aerobic, gram-positive rod. It forms spores, which can survive for years in the environment. Three clinical forms result after exposure to anthrax spores: cutaneous, respiratory, and gastro- intestinal. The cutaneous anthrax commonly prevails among humans. The respiratory form occurs most likely due to inhalation of the bacterial spores, whereas the gastrointestinal form happens after spores' ingestion. Prophylactic, early diagnosis and proper treatment will reduce mortalities of anthrax. Thus, the physicians, senior nurses and individuals at risk should be aware of the danger of this disease.
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ABSTRACT: We have isolated Clostridium perfringens type B, an epsilon toxin-secreting bacillus, from a young woman at clinical presentation of Multiple Sclerosis (MS) with actively enhancing lesions on brain MRI. This finding represents the first time that C. perfringens type B has been detected in a human. Epsilon toxin's tropism for the blood-brain barrier (BBB) and binding to oligodendrocytes/myelin makes it a provocative candidate for nascent lesion formation in MS. We examined a well-characterized population of MS patients and healthy controls for carriage of C. perfringens toxinotypes in the gastrointestinal tract. The human commensal Clostridium perfringens type A was present in approximately 50% of healthy human controls compared to only 23% in MS patients. We examined sera and CSF obtained from two tissue banks and found that immunoreactivity to ETX is 10 times more prevalent in people with MS than in healthy controls, indicating prior exposure to ETX in the MS population. C. perfringens epsilon toxin fits mechanistically with nascent MS lesion formation since these lesions are characterized by BBB permeability and oligodendrocyte cell death in the absence of an adaptive immune infiltrate.PLoS ONE 10/2013; 8(10):e76359. DOI:10.1371/journal.pone.0076359 · 3.53 Impact Factor