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Anthrax
DR. ANVESH NARIMETI INTERNALMEDICINE
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• The anthrax bacillus, Bacillus anthracis, was the first bacterium shown to be the cause of a disease
• In 1877, Robert Koch grew the organism in pure culture, demonstrated its ability to form endospores, and produced experimental anthrax by injecting it into animals
Introduction
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Introduction
• Bacillus anthracis is very large, Gram-positive, sporeforming rod
• Anthrax is caused by exposure to the spores of the bacteria Bacillus anthracis that become entrenched in the host body and produce lethal poisons
• It is primarily a disease of grazing animals such as cattle, sheep, goats, and horses
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The cells have characteristic squared ends. The endospores are ellipsoidal shaped and located centrally in the sporangium
It may exist as an individual bacterium or be grouped into short chains
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Anthrax bacteria in Gram stain
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Introduction
• The bacteria that cause anthrax are able to go into a dormant phase, in which they form spores.
• Spores can exist in the environment for decades.
• Under the right conditions, the dormant spores can germinate and multiply.
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• People of any age may be affected
• Humans are relatively resistant to cutaneous invasion by B anthracis, but the organisms may gain access through microscopic or gross breaks in the skin
Introduction
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• The organisms multiply locally and may spread to the bloodstream or other organs (eg, spleen) via the efferent lymphatics
• Dissemination from the liver, spleen, and kidneys back into the bloodstream may result in bacteremia
Introduction
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• B anthracis remains in the capillaries of invaded organs, and the local and fatal effects result due to the toxins elaborated
• Septicemic anthrax refers to overwhelming infection resulting from bloodstream invasion
Introduction
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PATHOGENESIS• Researchers found that there are three
proteins that are created by the anthrax bacteria.
• These proteins are harmless individually, but together can be deadly.
Protective antigen (PA) Edema factor (EF) Lethal factor (LF)
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• The edema factor, when combined with the protective antigen, forms a toxin known as the edema toxin ( EF + PA )
• The lethal factor, when combined with the protective antigen, forms a toxin known as the lethal toxin ( LF + PA )
PATHOGENESIS
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Frequency
• In the US: Natural incidence is rare
• Internationally: Anthrax used in bioterrorism ( ie, weapon-grade anthrax ) may be dispersed as an aerosol for mass effect or by focal spore contamination via letters or packages
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Mortality/Morbidity
• Most cases are cutaneous anthrax, are mild, and resolve with/without treatment
• However, other forms of anthrax are potentially fatal
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• Septicemic anthrax and inhalational anthrax highest mortality ( >90% )
• Intestinal anthrax higher mortality ( 20 - 60% )
• Cutaneous anthrax lowest mortality ( <1% )
Mortality / Morbidity
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Cutaneous anthrax ( 95% )
• occurs 1-7 days after skin exposure and penetration of spores
• Hematogenous dissemination occurs in 5-10% of untreated cases
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Cutaneous anthrax
• begins as a pruritic papule that enlarges in 24-48 hours to form an ulcer surrounded by a halo
• ulcer characteristically is pruritic but not painful
• painful Regional lymphadenopathy may occur
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• exudate of the ulcer contains numerous anthrax bacilli
• ulcer and surrounding edema evolve into a black eschar in 7-10 days and last for 7-14 days before separating and leaving a permanent scar
Cutaneous anthrax
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MALIGNANT
PUSTULE
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MALIGNANT
PUSTULE
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Oropharyngeal anthrax
• Ingestion of spores may result in oropharyngeal anthrax 2-7 days after exposure
• complain of unilateral sore throat/difficulty swallowing
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• proximal GI manifestation of intestinal anthrax
• accompanied by a membrane and is associated with local edema and cervical adenopathy
• Death may result from asphyxiation due to edema
Oropharyngeal anthrax
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Intestinal anthrax
• Ingesting spores may cause intestinal anthrax 2-5 days following ingestion
• complain of nausea, vomiting, malaise, anorexia, abdominal pain, hematemesis, and bloody diarrhea, which are accompanied by fever
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Intestinal anthrax
• Multiple anthrax ulcerative lesions are found throughout the GI tract secondary to hematogenous spread
• Intestinal anthrax is difficult to recognize, and shock and death may occur 2-5 days after onset
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Inhalational anthrax
• begins abruptly, 1-3 days after inhaling large concentrations of anthrax spores
• initially with nonspecific symptoms, low-grade fever and a nonproductive cough
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• substernal discomfort early in the illness
• progresses rapidly with high fever, severe shortness of breath, tachypnea, cyanosis, and chest pain, which may be so severe as to mimic an acute myocardial infarction
Inhalational anthrax
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Inhalational anthrax
• Chest percussion or radiographs reveal a widened mediastinum
• presents as hemorrhagic mediastinitis, not pneumonia, which may be associated with bloody pleural effusions
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Septicemic anthrax
• Internal organs become darkly colored with widespread petechiae and hemorrhage
• most cases of septicemic anthrax occur following inhalational anthrax
• massive amounts of lethal toxin result in shock and death
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Anthrax meningitis
• may complicate any form of anthrax
• bacteremia and hematogenous spread to the CNS
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• Cerebrospinal fluid (CSF) is distinguished by hemorrhagic leptomeningitis
• patients develop hemorrhagic leptomeningitis (Cardinal's cap)
Anthrax meningitis
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Causes
• Anthrax is caused by B anthracis, a gram-positive bacillus
• B anthracis produces a capsule that is easily visualized using a methylene blue or India ink stain
• Capsule formation may help differentiate B anthracis and other nonpathogenic bacilli.
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Lab Studies
• staining the ulcer exudate with methylene blue or Giemsa stain
• B anthracis readily grows on blood agar, and staining will microbiologically differentiate the organism and nonanthracis bacilli species
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Imaging Studies
• If inhalational anthrax is suspected, obtain a chest radiograph or CT scan
• a widening mediastinum appearance on chest x-ray/CT scan may suggest the diagnosis
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Other Tests
• B anthracis is present in high numbers in the ulcer/eschar of cutaneous anthrax, bloody pleural fluid, the CSF in anthrax meningitis, or the blood in septicemic anthrax
• Specimens may be stained/cultured to demonstrate the organism
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• Enzyme-linked immunosorbent assay (ELISA) serological diagnosis also is available
• If anthrax meningitis is suspected, obtain CSF for stain and culture.
• The CSF is grossly hemorrhagic with few PMN neutrophils
Other Tests
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Histologic Findings
• The characteristic finding in anthrax is the presence of the organisms in the capillaries at the infection site
• histology of inhalational anthrax is that of hemorrhagic mediastinitis
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Complications
• Septicemia
• Shock
• Hemorrhagic leptomeningitis
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Prognosis
• cutaneous anthrax - good prognosis
• inhalational anthrax - worst prognosis
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TREATMENT
• The preferred agent used to treat anthrax is penicillin
• Ampicillin (meningeal doses), doxycycline, and chloramphenicol penetrate the CSF, which is important in meningeal anthrax
• Use any quinolone for patients unable to take penicillin or doxycycline
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• Treatment ordinarily for 1-2 weeks
• Other antibiotics that may be useful include erythromycin, first-generation cephalosporins, chloramphenicol, clindamycin, vancomycin, carbapenems, cefoperazone, and extended-spectrum penicillins or trimethoprim-sulfamethoxazole (TMP-SMX)
TREATMENT
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postexposure prophylaxis
• Amoxicillin, doxycycline, or any quinolone (eg, ciprofloxacin, levofloxacin, gatifloxacin) for postexposure prophylaxis to prevent inhalation anthrax
• Postexposure prophylaxis should be continued for 60 days
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Prevention - Anthrax vaccine
• human anthrax vaccine in a dose of 0.5 mL subcutaneously, and
• repeat at 2 weeks and at 1, 6, 12, and 18 months following the initial immunization
• Administer a booster of 0.5 mL of human anthrax vaccine annually
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