Epidemiologic Study of a Fatal Case of Inhalation Anthrax

Fm, LaForce; Fh, Bumford; Jc, Feeley; Sl, Stokes; Db, Snow

doi:10.1080/00039896.1969.10665490

Cited by 37 publications

(14 citation statements)

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“…We have relearned and refined the basic histopathology and pathogenesis of anthrax, initially discerned from observations on humans (31,32) and in experimentally infected animals (11)(12)(13)(14)(15). This large series confirms previous reports of the pathologic changes in human inhalational anthrax (16 -21) but reveals the greater range of variation in the disease.…”

Section: Epidemiological and Clinical Variablessupporting

confidence: 56%

“…Immunohistochemical study revealed some IgM and/or IgG, but no complement, within some vessel walls; therefore, the distribution of these proteins may be a result of immunoglobulin leakage into damaged vessels, rather than causing the vasculitis. Vasculitis has not been reported in previous studies of human inhalational anthrax (11)(12)(13)(14)(15), nor was it identified in experimental studies (16 -21), but vasculitis and even microaneurysms were recognized by Russian workers, as significant constituents in the pathogenesis of intestinal anthrax; vascular injury was even postulated to be responsible for some of the hemorrhage observed (31). Derizhanov's (31) histopathologic observations of the lesions in autopsies of patients dying of intestinal anthrax were remarkably coincident with our observations, except that the primary site was distal small intestine and cecum with initial spread to mesenteric lymph nodes rather than the lungs and mediastinal lymph nodes, respectively, in these inhalational-anthrax cases.…”

Section: Epidemiological and Clinical Variablesmentioning

confidence: 98%

“…Inflammatory response was scant compared with the magnitude of necrosis/apoptosis, but neutrophils were prominent in patients with shorter survival, whereas mononuclear cells (large lymphocytes, immunoblasts, and macrophages) were significantly associated with longer survival. Previous reports of both human (11)(12)(13)(14)(15) and experimental (16 -21) inhalational and intestinal (31) anthrax variably report neutrophilic infiltrates associated with the hemorrhagic, necrotic tissue injury in anthrax; most descriptions include some, even significant, neutrophil infiltrates. Whereas the average magnitude of the neutrophil exudate in this series was low in most affected tissues, it was prominent in some locations in some cases and prominent in some organs, and not others, in other cases.…”

Section: Epidemiological and Clinical Variablesmentioning

confidence: 99%

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Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Abramova²,

et al. 2001

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Forty-one cases of documented inhalational anthrax from the Sverdlovsk epidemic of 1979 traced to release of aerosols of Bacillus anthracis at a secret biologic-agent production facility were evaluated by semiquantitative histopathologic analysis of tissue concentrations of organisms, inflammation, hemorrhage, and other lesions in the mediastinum, mediastinal lymph nodes, bronchi, lungs, heart, spleen, liver, intestines, kidneys, adrenal glands, and central nervous system. These data were correlated with clinical, epidemiologic, and demographic data.The patients' courses, with a variable incubation period and short nonspecific course (4 days before hospitalization) with rapid demise (1 day of hospitalization before death), correlated with systemic bacterial infection and lesions. Bacillus anthracis were identified in all cases in which there was no antibiotic treatment or there was treatment for fewer than 21 hours. The lesions that were the most severe and apparently of longest duration were in the mediastinal lymph nodes and mediastinum. There and elsewhere, peripheral transudate surrounded fibrin-rich edema; necrosis of arteries and veins was the most likely source of large hemorrhages displacing tissue or infiltrating tissue, respectively; and apoptosis of lymphocytes was observed. Respiratory function was compromised by mediastinal expansion, large pleural effusions, and hematogenous and retrograde lymphatic vessel spread of B. anthracis to the lung with consequent pneumonia. The central nervous system and intestines manifested similar hematogenous spread, vasculitis, hemorrhages, and edema. These pathologic findings are consistent with previous experimental studies showing transport of inhaled spores to mediastinal lymph nodes, where germination and growth lead to local lesions and systemic spread, with resulting edema and cell death, owing to the effects of edema toxin and lethal toxin. The identification of the vascular lesions as a basis for the prominent hemorrhages is a novel observation for human inhalational anthrax.

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Section: Epidemiological and Clinical Variablessupporting

confidence: 56%

Section: Epidemiological and Clinical Variablesmentioning

confidence: 98%

Section: Epidemiological and Clinical Variablesmentioning

confidence: 99%

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Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Abramova²,

et al. 2001

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“…B. anthracis spores can survive for several decades in the soil (23). Spores infect the host via intradermal inoculation, ingestion, or inhalation (6,12,14). After entry into the mammalian host, spores germinate and yield toxin-producing, capsulated bacilli.…”

mentioning

confidence: 99%

Polymorphism in the Collagen-Like Region of the Bacillus anthracis BclA Protein Leads to Variation in Exosporium Filament Length

Sylvestre¹,

Couture‐Tosi

Mock³

2003

J Bacteriol

167

180

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“…We therefore decided to study its sigB operon. Anthrax infection begins after inoculation, ingestion, or inhalation of spores, preventing exposure of the bacteria to stressful conditions immediately after entry into the host (29,45). Germination is required for establishment of the disease.…”

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confidence: 99%

Characterization of the Operon Encoding the Alternative ς ^B Factor from Bacillus anthracis and Its Role in Virulence

2000

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The operon encoding the general stress transcription factor B and two proteins of its regulatory network, RsbV and RsbW, was cloned from the gram-positive bacterium Bacillus anthracis by PCR amplification of chromosomal DNA with degenerate primers, by inverse PCR, and by direct cloning. The gene cluster was very similar to the Bacillus subtilis sigB operon both in the primary sequences of the gene products and in the order of its three genes. However, the deduced products of sequences upstream and downstream from this operon showed no similarity to other proteins encoded by the B. subtilis sigB operon. Therefore, the B. anthracis sigB operon contains three genes rather than eight as in B. subtilis. The B. anthracis operon is preceded by a B -like promoter sequence, the expression of which depends on an intact B transcription factor in B. subtilis. It is followed by another open reading frame that is also preceded by a promoter sequence similarly dependent on B. subtilis B . We found that in B. anthracis, both these promoters were induced during the stationary phase and induction required an intact sigB gene. The sigB operon was induced by heat shock. Mutants from which sigB was deleted were constructed in a toxinogenic and a plasmidless strain. These mutants differed from the parental strains in terms of morphology. The toxinogenic sigB mutant strain was also less virulent than the parental strain in the mouse model. B. anthracis B may therefore be a minor virulence factor.

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Epidemiologic Study of a Fatal Case of Inhalation Anthrax

Cited by 37 publications

References 13 publications

Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Polymorphism in the Collagen-Like Region of the Bacillus anthracis BclA Protein Leads to Variation in Exosporium Filament Length

Characterization of the Operon Encoding the Alternative ς ^B Factor from Bacillus anthracis and Its Role in Virulence

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Epidemiologic Study of a Fatal Case of Inhalation Anthrax

Cited by 37 publications

References 13 publications

Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Quantitative Pathology of Inhalational Anthrax I: Quantitative Microscopic Findings

Polymorphism in the Collagen-Like Region of the Bacillus anthracis BclA Protein Leads to Variation in Exosporium Filament Length

Characterization of the Operon Encoding the Alternative ς B Factor from Bacillus anthracis and Its Role in Virulence

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Characterization of the Operon Encoding the Alternative ς ^B Factor from Bacillus anthracis and Its Role in Virulence