Neurological and Physiological Responses of the Primate to Anthrax Infection

Klein, Frederick; Lincoln, Ralph E.; Dobbs, James P.; Mahlandt, Bill G.; Remmele, Norman S.; Walker, Jerry S.

doi:10.1093/infdis/118.1.97

Cited by 22 publications

(3 citation statements)

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“…Accidental or intentional exposure of B. anthracis spores by oral, cutaneous or pulmonary routes often triggers infection resulting in a high mortality rate associated with severe hypotension [2], [3], [4]. Treatment remedies such as administration of antibiotics, vaccination or antibody to the toxin have shown some promises in the clinical management of B. anthracis infection [1], [5].…”

Section: Introductionmentioning

confidence: 99%

Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism

Kandadi

Hua

et al. 2010

PLoS ONE

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ObjectivesAnthrax infection is associated with devastating cardiovascular sequelae, suggesting unfavorable cardiovascular effects of toxins originated from Bacillus anthracis namely lethal and edema toxins. This study was designed to examine the direct effect of lethal toxins on cardiomyocyte contractile and intracellular Ca2+ properties.MethodsMurine cardiomyocyte contractile function and intracellular Ca2+ handling were evaluated including peak shortening (PS), maximal velocity of shortening/ relengthening (± dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), intracellular Ca2+ rise measured as fura-2 fluorescent intensity (ΔFFI), and intracellular Ca2+ decay rate. Stress signaling and Ca2+ regulatory proteins were assessed using Western blot analysis.ResultsIn vitro exposure to a lethal toxin (0.05 – 50 nM) elicited a concentration-dependent depression on cardiomyocyte contractile and intracellular Ca2+ properties (PS, ± dL/dt, ΔFFI), along with prolonged duration of contraction and intracellular Ca2+ decay, the effects of which were nullified by the NADPH oxidase inhibitor apocynin. The lethal toxin significantly enhanced superoxide production and cell death, which were reversed by apocynin. In vivo lethal toxin exposure exerted similar time-dependent cardiomyocyte mechanical and intracellular Ca2+ responses. Stress signaling cascades including MEK1/2, p38, ERK and JNK were unaffected by in vitro lethal toxins whereas they were significantly altered by in vivo lethal toxins. Ca2+ regulatory proteins SERCA2a and phospholamban were also differentially regulated by in vitro and in vivo lethal toxins. Autophagy was drastically triggered although ER stress was minimally affected following lethal toxin exposure.ConclusionsOur findings indicate that lethal toxins directly compromised murine cardiomyocyte contractile function and intracellular Ca2+ through a NADPH oxidase-dependent mechanism.

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Section: Introductionmentioning

confidence: 99%

Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism

Kandadi

Hua

et al. 2010

PLoS ONE

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“…The loss of activity with the subcortical EEG corresponds with decreasing phrenic nerve discharge, a respiratory stimulus, and an ECG that suggests cardiac ischema (Vick et al, 1968). Similar effects occur when Rhesus macaques are challenged with B. anthracis Vollum spores (Klein et al, 1968). Since these experiments, there have been few publications in this area until a recent study that investigated the role of LT on the sympathetic nervous system.…”

Section: Neurological Effectsmentioning

confidence: 72%

Cellular and Physiological Effects of Anthrax Exotoxin and Its Relevance to Disease

Lowe¹,

Glomski²

2012

Front. Cell. Inf. Microbio.

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Bacillus anthracis, the causative agent of anthrax, secretes a tri-partite exotoxin that exerts pleiotropic effects on the host. The purification of the exotoxin components, protective antigen, lethal factor, and edema factor allowed the rapid characterization of their physiologic effects on the host. As molecular biology matured, interest focused on the molecular mechanisms and cellular alterations induced by intoxication. Only recently have researchers begun to connect molecular and cellular knowledge back to the broader physiological effects of the exotoxin. This review focuses on the progress that has been made bridging molecular knowledge back to the exotoxin’s physiological effects on the host.

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“…theria and peritonsillar abscess in the differential Alternatively death may occur secondary to a toxin diagnosis of inflammatory lesion of the oropharynx from B. anthracis, possibly through its suppression with neck swelling. If suspected, an appropriate of the respiratory centre (Klein et al, 1968). exposure history and bacteriological study can be In anthrax susceptible areas, oropharyngeal obtained and the diagnosis can be readily made.…”

Section: Discussionmentioning

confidence: 99%

Oropharyngeal anthrax

et al. 1985

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The first bacteriologically confirmed case of oropharyngeal anthrax is described. A 59-year-old male patient presented with sore throat and extensive swelling of the neck and anterior chest wall five hours after the ingestion of uncooked water buffalo meat. Marked inflammation of the oropharynx and a small necrotic area in the left tonsil were found. Culture taken from this area grew Bacillus anthracis. In anthrax-susceptible areas, this acute illness should be added to the differential diagnoses of inflammatory lesion of the oropharynx with extensive neck swelling.

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Neurological and Physiological Responses of the Primate to Anthrax Infection

Cited by 22 publications

References 1 publication

Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism

Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism

Cellular and Physiological Effects of Anthrax Exotoxin and Its Relevance to Disease

Oropharyngeal anthrax

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