There are three main types of anthrax infection:
Cutaneous anthrax
Cutaneous anthrax results from direct contact with the microbe on the skin or mucous membranes. More than 95% of naturally occurring anthrax is the cutaneous form. Approximately 1 to 7 days after anthrax endospores are introduced into the skin at a site of a previous cut or abrasion, a painless, pruritic macule or papule appears. Within 24 to 36 hours, the lesion forms a vesicle filled with clear or serosanguinous fluid containing numerous organisms that can be seen with Gram stain. The lesion undergoes necrosis, forming a painless ulcer covered by a characteristic central black eschar. There is accompanying non-pitting edema, which may be extensive, and multiple bullae may occasionally develop. Low-grade fever and malaise may be present, and painful regional lymphadenopathy can occur. Incision and debridement of early lesions should be avoided, since this may increase the chance of bacteremia. The eschar dries and falls off in 1 to 2 weeks, often with no residual scarring. The administration of antibiotics does not change the course of eschar formation but does decrease the likelihood of systemic disease. Although bacteremia is rare, the mortality rate has been reported to be as high as 20% without antibiotics but is less than 1 % with them.
Inhalational anthrax
Inhalational anthrax follows deposition of endospores into the alveolar spaces and may be a biphasic illness. The minimum infectious inhaled dose has not been precisely determined. Symptoms can develop 2 to 60 days after the inhalation of spores but usually develop after 6 days of incubation. The early phase is characterized by the insidious onset of fever, malaise, nonproductive cough, and dyspnea. Nausea, vomiting, and abdominal pain may also be present. Pleuritic chest pain and drenching sweats were prominent features in the 2001 U.S. anthrax outbreak. This stage of illness lasts from hours to a few days. Some patients may experience a brief period of apparent recovery. However, a second phase begins abruptly with spiking fevers, worsening dyspnea, and hypotension. A widened mediastinum due to massive mediastinal lymphadenopathy may be identified on chest radiograph. Pleural effusions may also be evident. These enlarged nodes can lead to partial tracheal compression and stridor. Up to one half of patients develop hemorrhagic meningitis with subsequent coma. Death can occur within hours. The mortality rate was previously reported to approach 90%, but in the recent U.S. anthrax bioterrorist cases, lower mortality rates (approximately 40%) were observed.
Gastrointestinal anthrax
Gastrointestinal anthrax can occur following the deposition of endospores in the upper or lower gastrointestinal tract. It is presumed that endospores inoculate areas of mucosal breakdown. This form of anthrax has never been reported in the United States. Symptoms can appear 2 to 5 days after the ingestion of endospore-contaminated meat. If spores are deposited in the oropharyngeal region, clinical findings typically include oral or esophageal ulceration accompanied by cervical edema and lymphadenopathy. Patients may complain of dysphagia, nausea, vomiting, fever, and even respiratory difficulty. Lesions have the appearance of pseudomembranous ulceration. If endospores are deposited in the lower gastrointestinal tract, patients may present with nausea, abdominal pain, fever, and bloody diarrhea. Hemorrhagic mesenteric lymphadenitis and massive ascites can also occur. Death occurs from intestinal perforation and anthrax toxemia. The case-fatality rate of gastrointestinal anthrax ranges from 12% to 50%.
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CLINICAL MANIFESTATIONS OF ANTHRAXThere are three main types of anthrax infection:Cutaneous anthraxCutaneous anthrax results from direct contact with the microbe on the skin or mucous membranes. More than 95% of naturally occurring anthrax is the cutaneous form. Approximately 1 to 7 days after anthrax endospores are introduced into the skin at a site of a previous cut or abrasion, a painless, pruritic macule or papule appears. Within 24 to 36 hours, the lesion forms a vesicle filled with clear or serosanguinous fluid containing numerous organisms that can be seen with Gram stain. The lesion undergoes necrosis, forming a painless ulcer covered by a characteristic central black eschar. There is accompanying non-pitting edema, which may be extensive, and multiple bullae may occasionally develop. Low-grade fever and malaise may be present, and painful regional lymphadenopathy can occur. Incision and debridement of early lesions should be avoided, since this may increase the chance of bacteremia. The eschar dries and falls off in 1 to 2 weeks, often with no residual scarring. The administration of antibiotics does not change the course of eschar formation but does decrease the likelihood of systemic disease. Although bacteremia is rare, the mortality rate has been reported to be as high as 20% without antibiotics but is less than 1 % with them.
Inhalational anthraxInhalational anthrax follows deposition of endospores into the alveolar spaces and may be a biphasic illness. The minimum infectious inhaled dose has not been precisely determined. Symptoms can develop 2 to 60 days after the inhalation of spores but usually develop after 6 days of incubation. The early phase is characterized by the insidious onset of fever, malaise, nonproductive cough, and dyspnea. Nausea, vomiting, and abdominal pain may also be present. Pleuritic chest pain and drenching sweats were prominent features in the 2001 U.S. anthrax outbreak. This stage of illness lasts from hours to a few days. Some patients may experience a brief period of apparent recovery. However, a second phase begins abruptly with spiking fevers, worsening dyspnea, and hypotension. A widened mediastinum due to massive mediastinal lymphadenopathy may be identified on chest radiograph. Pleural effusions may also be evident. These enlarged nodes can lead to partial tracheal compression and stridor. Up to one half of patients develop hemorrhagic meningitis with subsequent coma. Death can occur within hours. The mortality rate was previously reported to approach 90%, but in the recent U.S. anthrax bioterrorist cases, lower mortality rates (approximately 40%) were observed.
Gastrointestinal anthraxGastrointestinal anthrax can occur following the deposition of endospores in the upper or lower gastrointestinal tract. It is presumed that endospores inoculate areas of mucosal breakdown. This form of anthrax has never been reported in the United States. Symptoms can appear 2 to 5 days after the ingestion of endospore-contaminated meat. If spores are deposited in the oropharyngeal region, clinical findings typically include oral or esophageal ulceration accompanied by cervical edema and lymphadenopathy. Patients may complain of dysphagia, nausea, vomiting, fever, and even respiratory difficulty. Lesions have the appearance of pseudomembranous ulceration. If endospores are deposited in the lower gastrointestinal tract, patients may present with nausea, abdominal pain, fever, and bloody diarrhea. Hemorrhagic mesenteric lymphadenitis and massive ascites can also occur. Death occurs from intestinal perforation and anthrax toxemia. The case-fatality rate of gastrointestinal anthrax ranges from 12% to 50%.*207/348/5*

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